A videotape analysis of toddlers suggests that children's early knowledge about language structure is more limited than has been previously claimed [PNAS, 106(41):17284-17289].

Scientific opinions vary on how children go from uttering their first words to participating fully in verbal communication.

Some researchers suggest that toddlers start life with a general set of grammatical rules similar to adult recognition of language elements like word order; others believe that an infant's knowledge is limited and becomes more general later in life. After analyzing 28 hours of taped toddler speech, Colin Bannard, PhD, an assistant professor in the Department of Linguistics at the University of Texas in Austin and colleagues report that toddlers operate with concrete words and phrases and are only capable of using limited abstractions.

The authors reviewed the verbal traits of two 2-year-old toddlers and computed a set of rules for the composition of words and language structure based on the language each child produced. The rules provide a potential explanation for the toddlers' language.

A year later, however, the same rules were not effective at explaining the children's speech patterns. Toddlers may acquire a language gradually, based initially on specific vocabularies rather than general rules, according to the researchers.

The belief that healthy older brains are substantially smaller than younger brains may stem from studies that did not screen out people whose undetected, slowly developing brain disease was killing off cells in key areas, according to new research. As a result, previous findings may have overestimated atrophy and underestimated normal size for the older brain [Neuropsychology, 23(5): 541-550].

The new study tested participants in Holland's long-term Maastricht Aging Study who were free of neurological problems such as dementia, Parkinson's disease or stroke. Once participants were deemed otherwise healthy, they took neuropsychological tests, including a screening test for dementia, at baseline and every three years afterward for nine years.

According to the report participants were also given MRI scans at Year 3 to measure seven different parts of the brain, including the memory-laden hippocampus, the areas around it, and the frontal and cingulate areas of the cognitively critical cortex.

After examining behavioral data collected from 1994 to 2005 (with scans taken between 1997 and 1999 depending on when people entered the study), the researchers divided participants into two groups: one group with 35 cognitively healthy people who stayed free of dementia (average starting age 69.1 years), and the other group with 30 people who showed substantial cognitive decline but were still dementia-free (average starting age 69.2 years).

That cognitive decline was measured by drops of at least 30 percent on two or more of six core tests of verbal learning and fluency, recall, processing speed, and complex information processing, and/or drops of 3 or more points, or scores of 24 or lower (raising suspicion for cognitive impairment), on the Mini-Mental State Examination screening tool for dementia.

In contrast to the 35 people who stayed healthy, the 30 people who declined cognitively over nine years showed a significant effect for age in the hippocampus and parahippocampal areas, and in the frontal and cingulate cortices. In short, among the people whose cognition got worse, older participants had smaller brain areas than younger participants.

Thus, the seeming age-related atrophy in gray matter more likely reflected pathological changes in the brain that underlie significant cognitive decline than aging itself, the authors wrote. As long as people stay cognitively healthy, the researchers believe that the gray matter of areas supporting cognition might not shrink much at all. "If future longitudinal studies find similar results, our conception of 'normal' brain aging may become more optimistic," said lead author Saartje Burgmans, who is due to receive her PhD later this year.

The findings should caution scientists about drawing conclusions from brain studies that don't screen participants over time, using precise and objective definitions, the authors added.

Other study authors included: Martin P. J. van Boxtel, PhD, MD, Eric F. P. M. Vuurman, PhD, Floortje Smeets, PhD student, and Ed H. B. M. Gronenschild, PhD, Maastricht University; Harry B. M. Uylings, PhD, Maastricht University and VU University Medical Center Amsterdam; and Jelle Jolles, PhD, Maastricht University.

In laying down the neural circuitry of the developing brain, billions of neurons must first migrate to their correct destinations and then form complex synaptic connections with their new neighbors.

When the process goes awry, neurodevelopmental disorders such as mental retardation, dyslexia or autism may result. Researchers at the University of North Carolina at Chapel Hill School of Medicine have now discovered that establishing the neural wiring necessary to function normally depends on the ability of neurons to make finger-like projections of their membrane called filopodia [Cell, 138 (5):990-1004].

The finding indicates that the current notion regarding how cells change shape, migrate or differentiate needs to be revisited.

Scientists have thought that the only way for a cell to morph and move is through the action of the cytoskeleton or the scaffold inside the cell, pushing membrane forward or sucking it in, said senior study investigator Franck Polleux, PhD, associate professor in the Department of Pharmacology and the UNC Neuroscience Center at the UNC School of Medicine.

But Dr. Polleux's study shows that the brain protein srGAP2 can also impose cell shape by directly bending membranes, forming filopodia as a mean to control the migration and branching of neurons during brain development.

srGAP2 is one of a family of proteins that have been implicated in a severe mental retardation syndrome called the 3p- syndrome. Therefore this research could also yield important insights into the underlying causes of this and other forms of mental retardation.

Dr. Polleux and his colleagues began looking at srGAP2 because the gene was almost exclusively "turned on" or expressed during brain development. The brain protein contains a unique combination of domains - small functional chunks of protein sequence that may be common to other proteins as well. The star of these domains is one called the F-BAR domain, one of a handful of similarly termed "BAR domains" that have recently become a hotbed of research.

The UNC researchers were among the first to master a laboratory technique that enabled them to manipulate which genes are turned on or off in neurons, a notoriously difficult cell type.

Working with slices of mouse brain, they used electrical current to introduce pieces of genetic material that would either ramp up or, conversely, knock down the action of the protein's F-BAR domain. They then cultured brain slices in petri dishes allowing researchers to watch how the neurons behaved 'in the wild' in their native environment. When the researchers ramped up the activity of the domain, they saw that the neurons formed the finger-like filopodia which blocked migration by inducing too many branches.

"The textbook notion is that F-BAR proteins fold inward, but here we show it can do the opposite" said Dr. Polleux. "This is a completely novel mechanism for producing filopodia."

The researchers then found that when they reduced the expression of this protein, the neurons migrated at a faster rate and branched less. Under a microscope, neurons move like little inchworms. In front, the long thin cellular protrusion of the neuron extends, pauses, then drags the bulbous cell body behind it, then extends again, and so on.

Dr. Polleux says the F-BAR domain of srGAP2 appears to tightly control the amount of branching neurons undergo so they can be more streamlined when they need to migrate, and branch when they need to establish connections with other neurons.

Because disruptions in these critical connections would have detrimental effects on brain development, Dr. Polleux will now collaborate with clinicians at UNC to determine whether mutations in the srGAP2 gene are involved in autism or in other forms of mental retardation in addition to the 3p- syndrome. His laboratory also is interested in determining the function of approximately 25 other genes containing F-BAR-like domains, many of which are expressed in the developing brain.

Funding for the studies led at UNC came from the National Institutes of Health and the Pew Charitable Trusts. Study co-authors from UNC include Sabrice Guerrier, PhD, former graduate student; Jaeda Coutinho-Budd, graduate student; Takayuki Sassa, PhD, former postdoctoral fellow; Aurélie Gresset, graduate student; and Nicole Vincent Jordan, graduate student.

Chronic periodontitis, a form of gum disease, is an independent risk factor for head and neck squamous cell carcinoma. A new study suggests the need for increased efforts to prevent and treat periodontitis as a possible means to reduce the risk of this form of cancer [Cancer Epidemiology, Biomarkers & Prevention, 18 (9):2406-2412].

"Prevent periodontitis; if you have it already, get treatment and maintain good oral hygiene," said Mine Tezal, DDS, PhD, assistant professor in the Department of Oral Diagnostic Sciences, School of Dental Medicine, University at Buffalo, and NYS Center of Excellence in Bioinformatics and Life Sciences at the University of Buffalo and a research scientist in the Department of Dentistry and Maxillofacial Prosthetics at Roswell Park Cancer Institute, which is where the study was conducted.

Chronic periodontitis is characterized by progressive loss of the bone and soft tissue attachment that surround the teeth. The researchers assessed the role of chronic periodontitis on head and neck squamous cell carcinoma, as well as the individual roles on three subsites: oral cavity, oropharyngeal and laryngeal. They used radiographic measurement of bone loss to measure periodontitis among 463 patients; 207 of whom were controls.

Findings showed that chronic periodontitis might represent a clinical high-risk profile for head and neck squamous cell carcinoma. The strength of the association was greatest in the oral cavity, followed by the oropharynx and larynx, according to Dr. Tezal.

When they stratified the relationship by tobacco use, they found that the association persisted in those patients who never used tobacco. The researchers did not expect the periodontitis-head and neck squamous cell carcinoma association to be weaker in current smokers compared to former and never smokers, Dr. Tezal reported. However, this interaction, although statistically significant, was not very strong.

"Confirmatory studies with more comprehensive assessment of smoking, such as duration, quantity and patterns of use, as well as smokeless tobacco history are needed," she said. "Our study also suggests that chronic periodontitis may be associated with poorly differentiated tumor status in the oral cavity. Continuous stimulation of cellular proliferation by chronic inflammation may be responsible for this histological type. However, grading is subjective and we only observed this association in the oral cavity. Therefore, this association may be due to chance and needs further exploration."

High blood pressure is linked to memory problems in people over 45, according to recent research [Neurology, 73(8): 589-595].

The study found that people with high diastolic blood pressure, which is the bottom number of a blood pressure reading, were more likely to have cognitive impairment, or problems with their memory and thinking skills, than people with normal diastolic readings.

For every 10 point increase in the reading, the odds of a person having cognitive problems was seven percent higher. The results were valid after adjusting for other factors that could affect cognitive abilities, such as age, smoking status, exercise level, education, diabetes or high cholesterol.

The study involved nearly 20,000 people age 45 and older across the country who participated in the Reasons for Geographic And Racial Differences in Stroke (REGARDS) Study and had never had a stroke or mini-stroke. A total of 1,505 of the participants, or 7.6 percent, had cognitive problems, and 9,844, or 49.6 percent, were taking medication for high blood pressure.

High blood pressure is defined as a reading equal to or higher than 140/90 or taking medication for high blood pressure.

"It's possible that by preventing or treating high blood pressure, we could potentially prevent cognitive impairment, which can be a precursor to dementia," said study author Georgios Tsivgoulis, MD, of the University of Alabama at Birmingham.

Research has shown that high diastolic blood pressure leads to weakening of small arteries in the brain, which can result in the development of small areas of brain damage.

Dr. Tsivgoulis said more research is needed to confirm the relationship between high blood pressure and cognitive impairment.

The study was supported by the National Institute of Neurological Disorders and Stroke (NINDS).

"The REGARDS study is one of the largest population-based studies of risk factors for stroke. These latest data suggest that higher blood pressure may be a risk factor for cognitive decline, but further studies will be necessary to understand the cause-effect relationship," said Walter J. Koroshetz, MD, deputy director of NINDS and Fellow of the American Academy of Neurology. "The National Institutes of Health is now organizing a large clinical trial to evaluate whether aggressive blood pressure lowering can decrease a number of important health outcomes including cognitive decline."

Getting a cold, stomach bug or other infection may lead to increased memory loss in people with Alzheimer's disease, according to a new study [Neurology, 73(10): 768-774].

The study found that people who had respiratory, gastrointestinal or other infections or even bumps and bruises from a fall were more likely to have high blood levels of tumor necrosis factor-α, a protein involved in the inflammatory process, and were also more likely to experience memory loss or other types of cognitive decline than people who did not have infections and who had low levels of the protein.

The blood levels and cognitive abilities of 222 people with Alzheimer's disease with an average age of 83 were measured at the beginning of the study and three more times over six months. Caregivers were interviewed to determine whether the participants had experienced any infections or accidental injury that could lead to inflammation.

A total of 110 people experienced an infection or injury that led to inflammation during the study. Those people experienced memory loss that was at twice the rate of those who did not have infections or injuries.

People who had high levels of the protein in their blood at the beginning of the study, which may indicate chronic inflammation, had memory loss at four times the rate of those with low levels of the protein at the start of the study. Those who had high levels of the protein at the start of the study who also experienced acute infections during the study had memory loss at 10 times the rate of those who started with low levels and had no infections over the six-month period.

"One might guess that people with a more rapid rate of cognitive decline are more susceptible to infections or injury, but we found no evidence to suggest that people with more severe dementia were more likely to have infections or injuries at the beginning of the study," said study author Clive Holmes, MRCPsych, PhD, of the University of Southampton in the United Kingdom. "More research needs to be done to understand the role of tumor necrosis factor-alpha in the brain, but it's possible that finding a way to reduce those levels could be beneficial for people with Alzheimer's disease."

The study was supported by the Alzheimer's Society in London, UK.

More than 35 million people worldwide will have dementia in 2010, according to the 2009 World Alzheimer's Report from Alzheimer's Disease International (ADI). The new report was released on September 21st, which is World Alzheimer's Day.

This is a 10 percent increase over previous global dementia prevalence reported in 2005 in The Lancet. According to the new report, dementia prevalence will nearly double every 20 years, to 65.7 million in 2030 and 115.4 million in 2050.

According to researchers, the increases in global dementia prevalence were driven primarily by new data from low and middle income countries. Estimates for three regions are higher - Western Europe (7.29 percent vs. 5.92 percent), South Asia (5.65 percent vs. 3.40 percent) and Latin America (8.50 percent vs. 7.25 percent); East Asia is lower (4.98 percent vs. 6.46 percent) and North America is effectively identical.

The researchers found that 57.7 percent of people with dementia in 2010 live in low and middle income countries, rising to 70.5 percent by 2050. In addition, proportionate increases over the next 20 years in the number of people with dementia will be steeper in low and middle compared with high income countries.

"The information in the 2009 World Alzheimer's Report makes it clear that the crisis of dementia and Alzheimer's cannot be ignored," said ADI Executive Director Marc Wortmann. "Unchecked, Alzheimer's will impose enormous burdens on individuals, families, health care infrastructures, and global economy."

"There is hope in taking action by improving and funding dementia care and services, and increasing investment in research," he added. "Australia, France, Korea and the UK have developed national Alzheimer's action plans, and several more are currently in development. We strongly encourage other countries to follow their example and make Alzheimer's a priority."

The report also outlines challenges faced by governments and healthcare systems worldwide and offers eight global recommendations based on report findings.

The full 2009 World Alzheimer's Report, including the methodology used to prepare it, can be found at http://www.alz.co.uk/worldreport.  

Researchers from the UT Health Science Center San Antonio are delivering neuroprotective drugs to the brain in a mouse model of stroke by spraying them onto the lining of a nerve in the nose. The goal is to prevent the death of brain cells after stroke.

The drugs are delivered via the olfactory nerve, which controls the sense of smell. In humans, connections from this nerve extend to areas controlling speech, comprehension and opposite-side movement, all of which may be damaged by an ischemic stroke resulting in devastating disabilities. Ischemia is a lack of oxygen resulting from clots blocking blood vessels.

"This nerve is a highway to the brain through which we can easily deliver brain tissue-preserving agents, and we think this method of delivery may be good for eight to nine hours after a stroke begins," said David F. Jimenez, MD, professor and chairman of the Department of Neurosurgery at the Health Science Center.

Stroke, the nation's third-leading killer, can strike anyone at any time. As the minutes pass, brain tissues die from lack of oxygen. Tissue plasminogen activator (tPA), a clot-busting drug, is generally very effective if administered within the first three hours of stroke onset.

After three hours, surgery is often necessary to bust the clot or retrieve it. After six hours, it is difficult to limit stroke damage by any means. If aerosol drug delivery through the olfactory nerve can be moved from the mouse model to human clinical trials and eventually to federal approval, it would potentially expand that window.

Preliminary studies in the mouse model are extremely promising.

"This method offers direct access to the brain via topical application through the nose," said Murat Digicaylioglu, MD, PhD, assistant professor and director of neurosurgical research in the Department of Neurosurgery. "In mice it travels from the nose to crucial brain regions within 20 minutes. It is not affected by the blood-brain barrier, which prevents many drugs that are administered by injection from entering the brain."

In treated mice, the volume of brain tissue killed by stroke is two-thirds less than that of untreated mice, Dr. Digicaylioglu said.

"Most importantly, we have seen significant improvement in neurological outcome after stroke with this treatment, including motor function and behavioral measures such as ability to navigate a maze," he said.

If a clinical trial is conducted in the future and the delivery system is approved for use in humans, it is plausible to assume it could be carried aboard ambulances as a frontline therapy for immediate care of stroke patients. "This is a very exciting possibility," Dr. Jimenez said.

One day, if proven, the delivery system even could be used to administer therapies for Alzheimer's disease, Parkinson's disease and other neurodegenerative diseases, he said.

James Carlyle Marsters, DDS, a California orthodontist who was instrumental in the development of text telephones (TTYs), died comfortably in his sleep at his home in Oakland, CA on July 28, 2009. He was 85.

"He was an icon in my eyes," said Alan Hurwitz, president of the National Technical Institute for the Deaf (NTID), a college of Rochester Institute of Technology, who considered Dr. Marsters a personal friend for nearly 40 years. "He was like a father figure to me. He gave me wonderful advice and guidance whenever I needed to talk with him about anything. He was a very kind man, passionate and always interested in talking with people. He had a great sense of humor and was a man of many talents and interests. He will be sorely missed."

Dr. Marsters' most outstanding contribution to the Deaf community started in 1964, when he worked with two other deaf men, Robert Weitbrecht and Andrew Saks, to advocate for changes that would allow deaf persons to communicate with TTYs from home and work. Before that, deaf persons were limited to communication in person, by letters or by phone with the help of hearing friends or family members.

Chronicled in the book A Phone of Our Own: The Deaf Insurrection Against Ma Bell, by Harry G. Lang, Weitbrecht made history by calling Dr. Marsters with the first long distance TTY phone call on a traditional telephone line. Their communication was garbled at first. But after some adjustments were made, their typed words were clear and concise: "Are you printing me now?" Weitbrecht asked Dr. Marsters. "Let's quit for now and gloat over the success."

This teletype communication was made technically possible at that time by the development of an acoustic coupler that would carry signals through phone lines. The three men also worked to overcome the barriers to TTY communication established by telephone corporations, which at the time prohibited direct connections to telephone lines. They founded Applied Communications Corporation in Belmont, Calif. and obtained discarded teletype machines, repaired them and gave them to deaf people to use with the acoustic modems. They also educated the Deaf community about this new technology and partnered with other organizations to make TTYs a reality.

Thick telephone directories of TTY users were eventually published and local organizations were formed to allow deaf persons to meet, communicate and disseminate the technology across the country. TTYs liberated deaf persons, allowing them for the first time to independently communicate with others in different locations.

"I look back with pleasure and satisfaction with time well spent serving the public and fellow man," Dr. Marsters once said.

"My dad didn't want to draw the attention to himself, he wanted people to know it was a team effort," said his son, Jim Marsters Jr. "Even though he was the last of the three living (modem developers), he would tell people, 'The glory is not mine. It was an effort of many.' He was really modest about it, but it was something he was really, really proud of."

Dr. Marsters was a former member of the NTID National Advisory Group. He was presented with an honorary doctorate from RIT in 1996 and was honored in 2008 by having the modem he used for the first TTY call between two deaf persons prominently displayed at the RIT Wallace Memorial Library.

TDI (formerly Telecommunications for the Deaf and Hard of Hearing, Inc.) created the James C. Marsters Promotion Award for helping improve accessibility for people with disabilities.

"I just think about how he cared about other people - patients, family, friends in the deaf community," said his son. "When I was growing up, I remember he was spending a lot of time fussing around with those big Western Union teletype machines so you could communicate with another person who happened to have another machine on the other end. It started in his basement in Pasadena. But he spent a lot of time both in California and going to Washington pushing for government support for this program to make telephone communication more accessible to deaf people. I was really impressed by his time and energy he put in to help deaf people."

Born in Norwich, NY, Dr. Marsters became deaf as an infant. He graduated from the Wright Oral School for the Deaf in New York City in 1943 and earned a bachelor's degree in chemistry from Union College in Schenectady, N.Y. After graduating he moved to New York City and married Joan Tausik, a deaf painter.

He applied to dental schools but was repeatedly told a deaf person could not become a dentist. Undaunted after three years, he was eventually admitted to New York University College of Dentistry on a provisional basis with the understanding they would provide no special accommodations, his family said. He graduated with a DDS degree in 1952, becoming one of the first deaf dentists in the country.

After a divorce and a move to California, Dr. Marsters was admitted into a fellowship of orthodontics at the University of Southern California in Los Angeles, which he completed in 1954. He started a solo orthodontic practice in Pasadena in 1954 and continued until his retirement in 1990.

An accomplished pilot, Dr. Marsters had a second office in Lone Pine, Calif., where he would fly to in his private plane and provide dental services to their underserved community. Often those services were done for free because the patients could not afford dental care.

Although there were other deaf pilots, most would avoid flying to airports that required radio communication. Dr. Marsters, who spoke, radioed control towers and announced his proximity to the airport. He would ask the tower to give him clearance to land using signal lights, said his son.

In 1955, Dr. Marsters married Alice A. Dorsey, then the director of the preschool for deaf children at the John Tracy Clinic in Los Angeles. Together, they raised three children.

"They were an inseparable team through all of my father's accomplishments," said their daughter, Dr. Jean Marsters. "She supported him and was equally dedicated to issues of deaf advocacy and education as he was."

After 49 years of marriage, Alice died in 2003. He then moved from Pasadena to Oakland and remained active in that area's deaf community.

Dr. Marsters enjoyed fishing, sailing, soaring, genealogy, investing and roaming the country on family vacations in his motor home. He was a magician and appeared on a live television commercial in his college days.

He was active in both deaf and hearing communities - holding membership in the Masonic Lodge, Rotary and Kiwanis clubs and the American Dental Association. He served as vice-president of the Alexander Graham Bell Association for the Deaf and Hard of Hearing and was founding member of the Oral Deaf Adult Section of the association in 1964. He also was the association's first keynote convention speaker who was deaf. He was given the association's top award, "Honors of the Association" in 1990 for "extreme dedication to and sustained efforts to the betterment of the lives of people with hearing loss."

"Jim's passing has prompted innumerable reminisces from A.G. Bell members signifying the broad and deep impact he had on our lives," said A.G. Bell President John R. "Jay" Wyant, who cited his "indomitable can-do spirit" and persistent leadership. "He and the other pioneers of his generation were trailblazers in expanding communication access for individuals who are deaf or hard of hearing and their contributions touch us in many ways each and every day."

Dr. Marsters was a member of the National Advisory Group at NTID, where in 2000 he started the Dr. James C. Marsters Endowed Scholarship Fund to benefit deaf and hard-of-hearing students. He was presented with an honorary doctorate degree from RIT and in 2008 was honored when the modem used in the first TTY call between two deaf persons was prominently displayed in RIT's Wallace Memorial Library.

Dr. Marsters is survived by three children, Jim Marsters Jr. of Oakland, Dr. Jean Marsters and Guy Marsters, both of Pasadena, and two grandchildren.

Plans are being made for a memorial service in Oakland on Oct. 24 or 25. In lieu of flowers, the family suggests contributions may be made in his memory to the John Tracy Clinic, 806 West Adams Blvd., Los Angeles, CA 90007, or to the Jean Weingarten Peninsula Oral School, 3518 Jefferson Ave., Redwood City, CA 94062.

Contributions may also be made to the Dr. James C. Marsters Endowed Scholarship Fund, NTID Development Office, 52 Lomb Memorial Dr., Rochester, N.Y. 14623.

Possible neurological complications of heart surgery, ranging from headaches to strokes, are detailed in a new review article [MedLink Neurology, August 2009] by Betsy Love, MD, Sara Hocker, MD, and senior author Jose Biller, MD, of Loyola University Chicago Stritch School of Medicine.

In the review, the researchers list possible nervous system complications of bypass surgeries, aortic surgery, cardiac catheterizations, valve replacements, heart transplants and surgeries for congenital heart disease and heart tumors.

For example, possible complications from bypass surgery include vision problems, paralysis, hoarseness, movement disorders and disturbances in learning, memory, attention, concentration and mental agility. Depending on the patient's age, the operating techniques used and other factors, the risk of stroke ranges from just under 1 percent to as high as 5 percent, according to studies cited in the article.

"Neurologic complications of cardiac procedures can involve literally any part of the central and peripheral nervous systems," researchers wrote.

In 2006, 1.3 million angioplasties and 448,000 bypass surgeries were performed in the United States, according to the American Heart Association. Thousands of other patients underwent surgeries for other cardiac conditions.

Dr. Biller said that in cardiac surgery, there's always a risk of neurologic complications, especially in older patients who have other health problems.

However, he said patients should not be afraid to undergo cardiac procedures. Many complications are rare. And despite the risks, cardiac surgeries generally "are highly beneficial and life-saving," he said.

The article is an updated and fully revised version of a review article published in MedLink Neurology in June, 2008. The original article was written by Drs. Biller, Love and James Fleck, MD, of Indiana University School of Medicine.

The revised article includes a new section on aortic surgeries, such as aortic valve replacements. Complications of aortic surgery include stroke, paraplegia and peripheral nerve dysfunction. The new article also includes new sections on surgery to remove atrial myxomas (heart tumors) and surgery to close a hole in the heart called a patent foramen ovale.

Twice weekly acupuncture treatments relieve debilitating symptoms of xerostomia - severe dry mouth - among patients treated with radiation for head and neck cancer, researchers from The University of Texas M. D. Anderson Cancer Center report (Head & Neck Online, April 17, 2009).

Xerostomia develops after the salivary glands have been exposed to repeated doses of therapeutic radiation. People who have cancers of the head and neck typically receive large cumulative doses, rendering the salivary glands incapable of producing adequate saliva, said Mark S. Chambers, MS, DMD, a professor in the Department of Dental Oncology. Saliva substitutes, lozenges and chewing gum bring only temporary relief, and the commonly prescribed medication, pilocarpine, has short-lived benefits and bothersome side effects of its own.

"The quality of life in patients with radiation-induced xerostomia is profoundly impaired," said Dr. Chambers, the senior study author. "Symptoms can include altered taste acuity, dental decay, infections of the tissues of the mouth, and difficulty with speaking, eating and swallowing. Conventional treatments have been less than optimal, providing short-term response at best."

M. Kay Garcia, LAc, DrPH, a clinical nurse specialist and acupuncturist in the M. D. Anderson Integrative Medicine Program and the first study author, noted that patients with xerostomia may also develop nutritional deficits that can become irreversible.

Drs. Garcia, Chambers and their team of researchers conducted a pilot study to determine whether acupuncture could reverse xerostomia. Acupuncture therapy is based on the ancient Chinese practice of inserting and manipulating very thin needles at precise points on the body to relieve pain or otherwise restore health. In traditional Chinese medicine, stimulating these points is believed to improve the flow of vital energy through the body. Contemporary theories about acupuncture's benefits include the suggestion that needle manipulation stimulates natural substances that dilate blood vessels and increase blood flow to different areas of the body.

The study included 19 patients with xerostomia who had completed radiation therapy at least four weeks earlier. The patients were given two acupuncture treatments each week for four weeks. The acupuncture points used in the treatment were located on the ears, chin, index finger, forearm and lateral surface of the leg. All patients were tested for saliva flow and asked to complete self-assessments and questionnaires related to their symptoms and quality of life before the first treatment, after completion of four weeks of acupuncture, and again four weeks later.

The twice weekly acupuncture treatments produced highly statistically significant improvements in symptoms. Measurement tools included: the Xerostomia Inventory, asking patients to rate the dryness of their mouth and other related symptoms; and the Patient Benefit Questionnaire, inquiring about issues such as mouth and tongue discomfort; difficulties in speaking, eating and sleeping; and use of oral comfort aids. A quality-of-life assessment conducted at weeks five and eight showed significant improvements over quality-of-life scores recorded at the outset of the study.

"In this pilot study, patients with severe xerostomia who underwent acupuncture showed improvements in physical well-being and in subjective symptoms," Dr. Chambers said. "Although the patient population was small, the positive results are encouraging and warrant a larger trial to assess patients over a longer period of time."

Dr. Garcia said that a phase III, placebo-controlled trial is planned and is currently under review. She also noted that in other studies, the researchers are examining whether acupuncture can prevent xerostomia in patients treated for head and neck cancer, not just treat it.

"Recently, we completed a study at Fudan University Cancer Hospital in Shanghai, China that compared acupuncture to usual care to prevent xerostomia. We have now started a two-arm placebo-controlled pilot trial in Shanghai. In the prevention trials, acupuncture is performed on the same day as the radiation treatments," Dr. Garcia said.

In addition to Drs. Chambers and Garcia, other authors on the M. D. Anderson study include: Joseph S. Chiang, MD and Thomas Rahlfs, MD, Department of Anesthesiology and Pain Medicine; Lorenzo Cohen, PhD and Qi Wei, MS, Department of Behavioral Science/Integrative Medicine; Meide Liu, LAc, Place of Wellness; J. Lynn Palmer, PhD, Department of Palliative Care and Rehabilitation Medicine Research; David I. Rosenthal, MD, Department of Radiation Oncology; and Samuel Tung, MS and Congjun Wang, PhD, Department of Radiation Physics.

A Mayo Clinic-led international consortium has found a mechanism that may help explain Parkinson's and other neurological disorders [Nature Genetics, 41(2): 163-165].

Studying just eight families worldwide, the international team of researchers have discovered a genetic defect that results in profound depression and parkinsonism in a disorder known as Perry syndrome. Although this syndrome is exceedingly rare, the mechanism implicated in it may help explain the origins of a variety of neurodegenerative disorders, such as Parkinson's and amyotrophic lateral sclerosis diseases, and even common depression and sleep disorders that are also hallmarks of the disorder, the researchers say.

In the study, the researchers report that people with Perry syndrome have mutations in a subunit of the dynactin complex (DCTN1; p150glued), which is essential to the movement of molecular "cargo" inside brain cells, or neurons. In this case, the mutations meant that the cargo was being driven on a "train" that essentially had faulty brakes. And because Perry syndrome resembles many other neurodegenerative diseases, the findings suggest breakdowns along the cell's interior transportation grid may be a common mechanism underlying neurodegeneration.

"Understanding why distinct neurons are selectively vulnerable to neurodegeneration in different brain disorders is one of the greatest puzzles in neuroscience," says the study's lead investigator, Matthew J. Farrer, PhD, a professor of neuroscience at Mayo Clinic. "These findings suggest that trafficking of specific cargoes inside brain cells may be a general problem in a variety of neurodegenerative diseases, depression, and other disorders."

"It points us to a unified theory of what is going wrong in many of them," says the study's senior author, Zbigniew K. Wszolek, MD, professor of neurology at Mayo Clinic.

Molecules, vesicles and organelles within a cell are constantly carried via a network of crisscrossing microtubules that act like the tracks of an elaborate railroad system. Because, for the most part, neurons do not regenerate or divide as do other cells in the body, trafficking cargo efficiently over the lifetime of a neuron is fundamentally important, says Dr. Farrer.

Disruptions in this railroad system have been seen in many neurodegenerative diseases, but these problems have been generally regarded as byproducts of the disorder rather than the cause, the researchers say. These new findings may change that view, they say.

For example, in amyotrophic lateral sclerosis (ALS), a motor neuron disease also known as Lou Gehrig's disease, the molecular motors (for example, dynein, dynactin and kinesin) that drive transport from distant nerve terminals to the cell body may become defective. In some forms of Parkinson's disease, growing evidence indicates that the cargoes being trafficked are also misdirected by faulty signaling, due to pathogenic mutations in the leucine-rich repeat kinase 2(LRRK2) gene, Dr. Farrer says.

The findings may also shed light on other neurodegenerative disorders, the researchers say. In Alzheimer's disease, frontotemporal dementia and progressive supranuclear palsy, for instance, the "spikes," comprised of microtubule associated protein tau (MAPT), that normally stabilize and secure these rails tend to fall apart.

This discovery would not have been possible without a consortium of international researchers including co-authors from Canada, France, Japan, Turkey, and the United Kingdom, said Dr. Wszolek, who established the collaborative network of scientists.

Perry syndrome was first described in two unrelated Canadian families in 1975. In a study published in 2007, Dr. Wszolek, along with Swiss neurologist and visiting fellow Christian Wider, MD, summarized the clinical features of the disease, which include early-onset parkinsonism (stiffness, slowness and rigidity), depression, severe weight loss, and increasing difficulty in breathing. Once symptoms occur, typically in the patient's mid-40s, the disease is rapidly progressive and fatal.

In a subsequent study published in August 2008, the consortium reported that eight patients who died from the disease had substantial loss of neurons in the midbrain area known as the substantia nigra. They also found a molecular signature of Perry syndrome - "inclusions," or clumps, of a protein known as TDP-43 - which is found in patients with frontotemporal dementia or with motor neuron disease. What these clumps represent is not known, says co-author and neuropathologist Dennis Dickson, MD. "But they are clearly a marker of the disease process in all of these disorders, suggesting a common process is perturbed," he says.

Mayo geneticists hypothesized that Perry syndrome may be caused by mutations within the same gene, even though families afflicted with this disorder are unrelated, and come from different continents. The disease is autosomal dominant, meaning that the chance of inheriting the disease is 50 percent if one parent carries a copy of a mutant gene. With the help and participation of eight families with Perry syndrome, the Mayo-led team set out to find the defective gene.

They determined that each family had one of five novel mutations in the DCTN1 gene, whose protein produces a large subunit of the dynactin complex known as p150glued. This protein is essential to the movement of cargo along the microtubule rails. "Curiously, the mutations all cluster in the p150glued cytoskeleton-associated protein glycine-rich domain and its 'GKNDG' binding motif," Dr. Farrer said. "This region acts like a parking brake, so Perry mutations in p150glued mean that this brake is affected. It would be analogous to driving that train with faulty brakes."

What amazed the researchers are the similarities that Perry syndrome shares with other neurodegenerative diseases. Perry mutations in DCTN1 are physically very close to a mutation previously reported in familial motor neuron disease, they say.

The deposits of TDP43 are also the same as found in motor neuron disease and in some forms of frontotemporal dementia, although they are in a different part of the brain. "With the discovery of mutations in Perry syndrome, researchers have a new means to explore the breakdown in the microtubule transport system in each of these diseases," said Dr. Farrer. "The insides of neurons are very dynamic. Molecules and organelles are constantly being moved to where they are needed, so it makes sense that these disorders, with aging, may be caused by a progressive breakdown in this transport system."

Understanding Perry syndrome may shed light on depression as well as metabolic syndromes, said Dr. Wszolek. Many of the patients have profound depression and about one-third of those commit suicide. Many of the patients also experience severe weight loss and sleep deprivation.

The study was funded by the Pacific Alzheimer Research Foundation of British Columbia, Canada, and the National Institute of Neurological Disorders and Strokes, which funds the Morris K. Udall Parkinson's Disease Research Center of Excellence at Mayo Clinic, Jacksonville.

Individuals with clinical depression are less capable of finding pleasure in activities they previously enjoyed, a recent study has proven. Recent research shows reduced brain function in the reward center of the brain in depressed individuals, when compared to healthy subjects, [NeuroReport, 20(13):1204-1208].

The study was conducted by Elizabeth Osuch, MD, a researcher at the Lawson Health Research Institute, and is the first scientific publication of data obtained by the newly developed First Episode Mood & Anxiety Program (FEMAP) research arm at the London Health Sciences Centre in Ontario, Canada.

To investigate the effects of depression on brain activity, Dr. Osuch and her team asked 15 healthy subjects and 16 subjects who recently suffered from depression to provide a list of their favorite music as well as identify music that they neither liked nor disliked (neutral music). The subjects then listened to their musical selections for three minutes while a functional magnetic resonance imaging (fMRI) scanner measured the neural activity in their brain.

The researchers found that the healthy subjects showed more brain activity in specific regions when they listed to their favorite music compared to the subjects with depression. More specifically, several regions of the brain that are associated with reward processing were shown to be less activated in the individuals with depression, suggesting that even the most basic capacity of enjoyment seems to be malfunctioning in this area of the brain in those who have depression. This was true in spite of no difference in how enjoyable the two groups rated listening to the music in the scanner.

"Our results revealed significant responses within the areas of the brain that are associated with reward processing in healthy individuals. They also showed significant deficits in these neurophysiological responses in recently depressed subjects compared to the healthy subjects," explained Dr. Osuch. "It is known that depressed individuals experience anhedonia-a loss of enjoyment in previously pleasurable activities. The study results show that for recently depressed individuals this loss of enjoyment is linked to very specific parts of the brain which are involved with experiencing pleasure. If we can target these areas of the brain through treatment, we have the potential to treat depression earlier, right at the source."

Scientists have long suspected that Alzheimer's disease is caused by a small protein called the amyloid β-protein (Aβ). This protein clumps or binds to itself, eventually changing chemically to create brain protein deposits (plaques) that are characteristic of the disease. Recent studies have suggested that it is not the plaques that cause Alzheimer's, but rather these small, grape-like clusters of Aβ. These clusters vary in size, and the relationship between cluster size and their ability to kill nerve cells (toxicity) has never been determined accurately until now.

By creating various sizes of Aβ clusters in the lab that exactly match what forms in brains of those afflicted with Alzheimer's disease, neurologists at UCLA have determined that toxicity increases dramatically as clusters increase in size from two to three to four Aβs. The researchers also report that although the larger clusters are more toxic than smaller ones, the larger formations are relatively rare; smaller versions are numerous and thus are an inviting target for the development of new therapeutic drugs [PNAS Online, Aug. 12, 2009].

In addition, said David Teplow, PhD, senior author and a professor of neurology, developing the ability to make Aβ clusters in a very pure and precise way that duplicates what forms in brains with Alzheimer's will enable scientists to make detailed studies of their structures. This too will make development of future therapeutic drugs much easier and likely more successful.

Alzheimer's disease is the most common form of late-life dementia. More then five million Americans have been diagnosed with the disease, 24 million worldwide, and the numbers are expected to reach 81 million by the year 2040.

"We now have the best understanding yet of what types of toxic A-beta structures we should target with new classes of therapeutic drugs," said Dr. Teplow.

The researchers looked at the Aβ molecule, which is the chemical building block for structures that cause Alzheimer's. The molecule binds together, forming clusters of various sizes. The researchers found that the larger the cluster, the greater the toxicity, but they also found that the increase in toxicity with these clusters is not linear.

"Clusters that contain two Aβ molecules are more toxic than a single Aβ molecule, and those with three molecules are more toxic that those with two," said Dr. Teplow. But clusters of the Aβ molecule composed of dimers (two Ab molecules forming a cluster) are three-fold more toxic than the simple monomer compound, but trimers (with three Aβ molecules) and tetramers (four molecules) are more than 10-fold more toxic than are monomers, he said.

This suggests that the larger, more toxic clusters should be the target for scientists trying to stop Alzheimer's. Researchers noted that the relative amounts of the smaller clusters are far greater than that of the bigger clusters and are, in total, more toxic.

So in an Alzheimer's brain, the larger clusters are relatively rare. "Think of the molecules being wrapped in very weak Velcro," explained Dr. Teplow. "A number of molecules can bind together to form large clusters, but they break apart very easily."

Having developed a process in the lab to be able to make pure forms of these Aβ clusters of specific size will enable detailed study of their structures to show where every atom is. "This will make development of drugs much easier and likely more successful," he said.

Other authors included Kenjiro Ono of UCLA and Kanazawa University School of Medicine (Japan); and Margaret M. Condrona of UCLA. Funding was provided by the Japan Human Science Foundation, a Pergolide Fellowship from Eli Lilly Japan, the Mochida Memorial Foundation for Medical and Pharmaceutical Research, the National Institutes of Health, the Alzheimer's Association and the Jim Easton Consortium for Alzheimer's Drug Discovery and Biomarkers at UCLA.

House Ear Institute and House Ear Clinic neurologist Antonio De la Cruz, MD, passed away from complications from lymphoma at St. Vincent Medical Center in Los Angeles, California, on Friday morning, July 31, 2009, at the age of 65. He is survived by his son Anthony Charles, daughter Jeanette, and his longtime companion Milia Metos.

For the many people who knew him, Dr. De la Cruz will be remembered fondly as a kind and caring humanitarian, with a passion not only for helping patients with auditory disorders, but also as someone who cared deeply about sharing medical and scientific knowledge with the worldwide medical community. Over the course of his career, Dr. De la Cruz made a positive difference in the lives of thousands of people.

Dr. De la Cruz received his Doctorate in Medicine in 1967 and completed his specialty training in otolaryngology at the University of Miami Hospitals in 1973. After completing his Fellowship at the House Ear Clinic in Los Angeles in 1974, he joined the practice as an Associate in January 1975.

In addition to being a world-renowned neurotologist at the House Ear Clinic, Dr. De la Cruz served as the House Ear Institute Director of Education, leading professional training programs for hundreds of visiting physicians from around the world in otology/neurotology surgical procedures and practices. He also was an active member of the House Ear Institute's Board of Trustees since 1984.

"All of us at the House Clinic and House Ear Institute are saddened at the sudden passing of our dear friend and colleague Antonio De la Cruz. I have had the honor of working with Tony since we both arrived at the Institute in 1974," said John House, MD, president, House Ear Institute and associate, House Clinic. "He has given so much to so many people all of over the world. He enjoyed his patients and his teaching. He will be missed by all who have been touched by him."

His love of teaching extended beyond the institute and clinic to USC's Keck School of Medicine, where he served as a Clinical Professor of Otolaryngology - Head and Neck Surgery. Furthermore, as often as twice a month, Dr. De la Cruz would present the work of the House Ear Institute and House Ear Clinic at medical conferences in Europe, the South Pacific and North, Central and South America. His impeccable fluency in English, Spanish, Portuguese, Italian and French proved invaluable wherever he traveled.

Dr. De la Cruz was president of the Pan American Congress for 2002 and is a past president of the American Academy of Otolaryngology - Head and Neck Surgery and the American Otologic Society. He is a fellow of the American Otologic Society, American Laryngological Rhinological and Otological Society and American College of Surgeons. Over the course of his accomplished career, he authored numerous publications, journal articles and presentations.

Two studies conducted by researchers at the University of Illinois at Chicago and Northwestern University have found that commonly used botanicals do not have an effect on hot flashes or on cognitive function in menopausal women  

In the first study, the botanicals black cohosh and red clover were compared to the standard of care - hormone therapy - and to placebo for the treatment of hot flashes [Menopause Online, July 15, 2009].

The researchers enrolled 89 women with moderate to severe hot flashes in a four-arm, randomized, double-blind clinical trial. The women, who experienced at least 35 hot flashes and night sweats per week, were followed for 12 months. They kept diaries to record the number of hot flashes per day as well as the intensity.

The researchers found that the average number of hot flashes per week decreased over time across all groups - black cohosh decreased 34 percent, red clover 57 percent, placebo 63 percent and hormone therapy 94 percent.

"The important message is that all women improved, but there was a large placebo effect, and the botanicals did not work significantly better than placebo," said Stacie Geller, PhD, the G. William Arends Professor of Obstetrics and Gynecology at UIC and lead author of the study. "As expected, hormone therapy, considered the gold standard, significantly reduced hot flashes when compared with placebo," Dr. Geller said.

"We also found that the botanicals were safe - which is important, since many women will still continue to use them."

Dr. Geller and colleagues from the UIC/National Institutes of Health Center for Botanical Dietary Supplements Center reported no significant differences between botanical treatments and placebo for any of the safety parameters, including breast and endometrial safety, liver enzymes, complete blood count, or lipid profiles.

In a second study, UIC and Northwestern researchers enrolled 66 women from the parent trial to determine whether the botanic treatments had an effect on cognitive abilities, particularly verbal memory. It is the first study to evaluate the cognitive effects of black cohosh [Menopause Online, July 31, 2009].

The women completed baseline cognitive testing before receiving treatment and again during the 12-month treatment to measure the recollection of words and short stories. They also wore monitors that measured changes in skin conductance during a hot flash. Both subjective and objective hot flashes were recorded during a 24-hour period.

The study, like the main trial, found that none of the botanicals had either a beneficial or a detrimental effect on memory. The specific hormone therapy used in the trial, Prempro, had a slight negative impact on memory.

"Together, these two studies demonstrate that compared to botanicals, only hormone therapy had a beneficial effect on vasomotor symptoms, but this benefit was at the cost of a slight decrease in memory," said Pauline Maki, PhD, UIC associate professor of psychiatry and psychology and lead author of the cognition study. The focus of ongoing research at UIC, Dr. Maki said, is to identify a safe and effective treatment for hot flashes that is either neutral or beneficial to memory functioning.

Norman Farnsworth, PhD, who heads the UIC/NIH Botanical Center, notes that the center continues to study botanicals for their safety and efficacy in maintaining women's health and well-being. The center is supported by a grant from the NIH Office of Dietary Supplements, the NIH National Center for Complementary and Alternative Medicine, UIC, and the UIC College of Pharmacy. Additional support for the clinical trial came from the Naturex, Inc. of Hackensack, NJ and Pharmavite LLC of Mission Hills, CA.

Co-authors of the primary safety and efficacy study include Lee Shulman, Suzanne Banuvar and Geena Epstein of Northwestern University Feinberg School of Medicine, and Richard van Breemen, Ying Zhou, Samad Hedayat, Dejan Nikolic, Elizabeth Krause, Colleen Piersen, Judy Bolton, Guido Pauli and Farnsworth of UIC.

Co-authors of the cognitive study include Banuvar and Shulman of Northwestern and Leah Rubin, Deanne Fornelli and Lauren Drogos of UIC.

Being active at age 5 helps kids stay lean as they age even if they don't remain as active later in childhood, a new study from researchers at the University of Iowa (UI) in Iowa City shows [American Journal of Preventive Medicine, 37(1): 35-40].

"We call this effect 'banking' because the kids benefit later on, similar to having a savings account at a bank. The protective effect is independent of what happens in between," said lead author Kathleen Janz, EdD, professor of health and sport studies in the UI College of Liberal Arts and Sciences. "The implication is that even 5-year-olds should be encouraged to be as active as possible because it pays off as they grow older."

The researchers tested the body fat and activity level of 333 kids at ages 5, 8 and 11 using gold-standard technology: a special scanner that accurately measures bone, fat and muscle tissue, and an accelerometer that measures movement every minute. The kids wore accelerometers to record their activity level for up to five days, providing much more reliable data than relying on kids or parents to track minutes of exercise.

The study indicates that kids who are active at age 5 end up with less fat at age 8 and 11, even when controlling for their accumulated level of activity.

The average 5-year-old in the study got 30 minutes of moderate to vigorous exercise per day. For every 10 minutes on top of that, kids had one-third of a pound less fat tissue at ages 8 and 11.

Dr. Janz said further investigation is needed to learn what happens to the active kids' bodies that keeps them in better shape down the road. It may be possible that the active 5-year-olds didn't develop as many fat cells, improved their insulin response, or that something happened metabolically that provided some protection even as they became less active.

The study also indicated that boys are more likely to experience the sustained benefit from being active as preschoolers, possibly because they are more active at age 5 than girls, highlighting a need to especially encourage young girls to exercise.

"The CDC recommends that kids get at least 60 minutes of age-appropriate physical activity every day, and an activity like coloring madly won't cut it," Dr. Janz said.

The challenge is that it can be difficult to measure minutes of activity, since kids exert themselves in short bursts - think sprinting after a ball - rather than continuous activities, like jogging. So what can parents do?

"Avoid long periods - more than 60 minutes - of sedentary activity, insist that schools provide morning and afternoon recesses and whenever possible get kids outside. Kids who meet the CDC activity recommendations tend to be kids who spend a fair amount of time outdoors enjoying unstructured play," Dr. Janz said. "In the end, it doesn't take that much extra physical activity to see a measurable outcome. Even 10 extra minutes a day makes a difference in protecting against excessive fat gains."

Co-authors of the study included researchers from the UI departments of epidemiology, preventative and community dentistry, and pediatrics.

Severe chronic obstructive pulmonary disease (COPD) is associated with lower cognitive function in older adults, according to research from Mount Sinai School of Medicine in New York, NY [American Journal of Respiratory and Critical Care Medicine, 180(2): 134-137]

Researchers compared cognitive performance in over 4,150 adults with and without COPD and found that individuals with severe COPD had significantly lower cognitive function than those without, even after controlling for confounding factors such as comorbidities.

"Our findings should raise awareness that adults with severe COPD are at greater risk for developing cognitive impairment, which may make managing their COPD more challenging, and will likely further worsen their general health and quality of life," wrote lead author of the study, William W. Hung, MD, MPH, assistant professor at Mount Sinai School of Medicine.

Patients with COPD may experience periods of hypoxia-low oxygen levels-that might lead to brain abnormalities that could reduce cognitive capacity. Alternatively, hypoxia may cause or exacerbate diseases that are characterized by cognitive impairment, such as Alzheimer's disease. Although past studies have observed a higher rate of cognitive impairment among adults with COPD, the relationship has not been formally tested longitudinally in large populations until now.

"We wanted to determine whether the observed relationship between COPD and cognitive impairment was, in fact, something we could document over time, and if so, we wanted to determine whether the degree to which it occurred was significant," said Dr. Hung.

To do so, Dr. Hung and colleagues obtained data from the Health and Retirement Study, a national prospective biennial survey of Americans 50 and older. They included data from survey takers who had undergone cognitive testing in 1996 and again in 1998, 2000 or 2002.

Of the 4,150 individuals ultimately included, 492 had COPD, and of those, about one-third (153) had severe disease. Using a 35-point cognition scale, the researchers found that scores among all patients with COPD declined on average by one point over the six-year period between 1996 and 2002.

After further classifying those with COPD as having severe or nonsevere disease, the researchers found that severity and cognitive decline were linked. Even after controlling for sociodemographic characteristics and other confounding factors, the mean cognition scores for those with severe COPD were significantly lower (0.9 points; p=0.01) than those without COPD.

"These objective measures of cognition used in survey research do correlate with functional impairment," said Dr. Hung. In particular, executive functions that require greater cognitive ability, such as handling money and medications, are more poorly performed at greater levels of cognitive impairment. Extrapolating from past research using the same cognitive test, Dr. Hung and colleagues suggest that their findings would likely be associated with a 22 percent increase in the mean number of difficulties the severe COPD population would experience with daily tasks.

"While this number may not appear to be of major concern on the individual level, on a population level, it is roughly equivalent to nearly a quarter of severe COPD patients experiencing difficulty with a basic life skill," said Dr. Hung. "In this regard, these findings have serious implications. Often patients with cognitive difficulties, if undetected and untreated, have lower adherence to their treatment and follow-up regimens, and as a consequence may deteriorate more rapidly and have worse health outcomes."

In conclusion, Dr. Hung suggested that physicians and other clinical staff managing the care of these patients should be aware of their increased risk for cognitive decline and the greater needs and challenges associated with caring for cognitively impaired older adults.

Our tendency to see people and faces as individuals may explain why we are such experts at recognizing them, new research indicates. This approach can be learned and applied to other objects as well (Psychological Science, in press).

"This new research adds to the evidence that the brain processes faces differently because of our expertise with them. It also tells us what it is about our experience with faces that leads us to treat them holistically," Isabel Gauthier, PhD, associate professor of psychology at Vanderbilt University in Nashville, TN, and one of the study co-authors, said. "This knowledge may be useful in the development of training protocols for individuals with difficulties in face perception, such as individuals with autism spectrum disorders."

The research is currently in press at Psychological Science. Gauthier's co-authors are Alan Wong, PhD, who completed the study as his doctoral thesis in psychology at Vanderbilt, and Thomas Palmeri, PhD, associate professor of psychology. Dr. Wong is now an assistant professor at Chinese University of Hong Kong.

"Our findings suggest that facial expertise does not just develop with any type of experience," he said. "Learning to recognize a set of objects as individuals may work, but categorizing them at a more general level, or learning to manipulate them, would not. We develop different types of expertise in recognizing different objects not just due to their unique appearance, but also because of the types of experience we have had with them."

For decades, scientists have debated whether we are better able to recognize faces because we have evolved a brain system dedicated to this task or because we have extensive practice recognizing faces. Researchers agree that we recognize faces holistically, which is not how we generally recognize other objects. For example, we find it almost impossible to attend to only one part of a face and ignore the rest, while we might recognize a car by its grill, taillights or branding.

Prior research has shown that people can develop face-like expertise with novel objects, such as cars, and that once that expertise has been developed those objects are also processed holistically. But up until now it was unclear what it was about expertise that produced this holistic effect.

In the new study, Drs. Wong, Gauthier and Palmeri investigated this question by comparing two different types of training regimens with the same novel objects, called Ziggerins. The Ziggerins were created just for the experiment and have no real-world function.

One group learned to individuate these objects with unique names, much like we do with people and faces. Another group learned to very quickly categorize the objects based on shared structure. Each group became better than the other at the task on which it was trained, illustrating that different kinds of perceptual expertise can develop for the same objects. But, only the group that learned to individuate Ziggerins later processed novel Ziggerins holistically, like faces.

"This research indicates that not only is individuation key to our expertise with faces, but that this technique can be quickly applied to other objects," the authors wrote. "Hallmarks of face-like expertise do not require 10 years, or even 10 hours, of experience to emerge."

The research was supported by grants from the James S. McDonnell Foundation and the National Science Foundation and was conducted as a project of the National Science Foundation-funded Temporal Dynamics Learning Center.

A conference hosting leading experts in the fields of psychology, cognitive sciences, and speech and hearing sciences, convened a three-day conference in late July on the impact of executive function on education and developmental outcomes, specifically in children and adults who are deaf or hard of hearing.

The conference, entitled the "Listening and Spoken Language Symposium," was sponsored by the Alexander Graham Bell Association for the Deaf and Hard of Hearing (AG Bell). The symposium focused on executive function which is defined as the cognitive, or thinking, process that begins in infancy and continues through early childhood, adolescence and young adulthood. Executive function involves the global coordination, integration and functional connectivity of multiple underlying brain systems used in speech perception and production, and spoken language development.

"Executive function has become one of the most critical concepts to understand in the field of child development," said John R. "Jay" Wyant, president of AG Bell. "Recent developments in the research and medical fields have unlocked many secrets as to how the brain works and how we 'learn how to learn.'"

The symposium ran from July 23 to July 25 and featured two pre-conference short courses, two general sessions, two panel discussions and eight workshops focusing on executive function and the development of problem-solving skills, social competence and academic readiness.

Keynote speakers included Kimberly Andrews Espy, PhD, associate vice chancellor for research and a professor in the department of Psychology at the University of Nebraska at Lincoln; and David B. Pisoni, PhD, chancellors' professor of Psychology and Cognitive Science, and director of the Speech Research Laboratory at Indiana University.

Symposium attendees included teachers of the deaf, speech language pathologists, listening and spoken language specialists, audiologists, and researchers and clinicians.

"This symposium is designed to first, educate us on executive function and the impact a hearing loss can have on how a child's executive function develops, and second, to exchange information about real-world applications," said Wyant, who was born profoundly deaf. "We are very excited to be able to offer this high-quality program focused on one of the most cutting-edge issues in listening and spoken language development today."

Participating in certain mental activities, like reading magazines or crafting in middle age or later in life, may delay or prevent memory loss, according to results of a study presented at the American Academy of Neurology 61st Annual Meeting in Seattle, in April.

The study involved 197 people between the ages of 70 and 89 with mild cognitive impairment, or diagnosed memory loss, and 1,124 people that age with no memory problems. Both groups answered questions about their daily activities within the past year and in middle age, when they were between 50 to 65 years old.

The study found that during later years, reading books, playing games, participating in computer activities and doing craft activities such as pottery or quilting led to a 30 to 50 percent decrease in the risk of developing memory loss compared to people who did not do those activities. People who watched television for less than seven hours a day in later years were 50 percent less likely to develop memory loss than people who watched for more than seven hours a day.

People who participated in social activities and read magazines during middle age were about 40 percent less likely to develop memory loss than those who did not do those activities.

"This study is exciting because it demonstrates that aging does not need to be a passive process. By simply engaging in cognitive exercise, you can protect against future memory loss," said study author Yonas Geda, MD, MSc, a neuropsychiatrist at Mayo Clinic in Rochester, MN. "Of course, the challenge with this type of research is that we are relying on past memories of the participants, therefore, we need to confirm these findings with additional research."

The study was supported by the National Institutes of Health, Robert H. and Clarice Smith and Abigail Van Buren Alzheimer's Disease Research Program and the Robert Wood Johnson Foundation.

Gesturing helps students develop new ways of understanding mathematics, according to research at the University of Chicago [Psychological Science, 20 (3): 267-272].

Scholars have known for a long time that movements help retrieve information about an event or physical activity associated with action. This research is the first to show that gestures not only help recover old ideas, they also help create new ones. The information could be helpful to teachers, scholars said.

"This study highlights the importance of motor learning even in nonmotor tasks, and suggests that we may be able to lay the foundation for new knowledge just by telling learners how to move their hands," writes lead author and psychologist Susan Goldin-Meadow, PhD.

Dr. Goldin, Meadow, the Beardsley Ruml Distinguished Service Professor in Psychology, was joined by Susan Wagner Cook, PhD, now assistant professor of Psychology a the University of Iowa and University of Chicago research assistant Zachary Mitchell, in writing the article and doing the research.

For the study, 128 fourth-grade students were given problems of the type 3+2+8=__+8. None of the students had been successful in solving that type of problem in a pre-test. The students were randomly divided into three instruction groups.

One group was taught the words, "I want to make one side equal to the other side." Another group was taught the same words along with gestures instantiating a grouping problem-solving strategy - a V-shaped hand indicating 3+2, followed by a point at the blank (group and add 3 and 2 and put the sum in the blank). A third group was taught the words along with gestures instantiating the grouping strategy but focusing attention on the wrong numbers - a V-shaped hand indicating 2+8, followed by a point at blank. The experimenter demonstrating the gesture did not explain the movement or comment about it.

All of the students were then given the same mathematics lesson. On each problem during the lesson, they were told to repeat the words or words/gestures they had been taught.

After the lesson, students were given a test in which they solved new problems of this type and explained how they reached their answers. Students who repeated the correct gesture during the lesson solved more problems correctly than students who repeated the partially correct gesture, who, in turn, solved more problems correctly than students who repeated only the words.

The number of problems children solved correctly could be explained by whether they added the grouping strategy to their spoken repertoires after the lesson, Dr. Goldin-Meadow said. Because the experimenter never expressed the grouping strategy in speech during the lesson, and students picked it up on their own as a new idea, the study demonstrates that gesture can help create new concepts in learning.

"The grouping information students incorporated into their post-lesson speech must have come from their own gestures," Dr. Goldin-Meadow said.

"Children were thus able to extract information from their own hand movements. This process may be the mechanism by which gesturing influences learning," she said.

A new study shows that people who are smokers and have a family history of brain aneurysm appear to be significantly more likely to suffer a stroke from a brain aneurysm themselves [Neurology, 72(1):69-72].

The type of stroke, called subarachnoid hemorrhage, is one of the bleeding types of stroke and is deadly in about 35 to 40 percent of people.

In the study, scientists looked at 339 people who suffered a stroke from a brain aneurysm and 1,016 people who had not had a stroke due to an aneurysm. Current smokers made up half of the group that had a stroke. The other half had never smoked or had smoked in the past.

The research found people who smoked and had a family history of stroke were more than six times more likely to suffer a stroke than those who did not smoke and did not have a family history of stroke or brain aneurysm. The study also found that people with a family history of stroke could cut their risk by more than half by quitting smoking. The results were the same regardless of high blood pressure, diabetes, alcohol use, body mass index and education level.

"While all people should be advised to quit smoking, our findings suggest that there is an interaction so that if you smoke and you have a family history of aneurysms, you are at an extremely high risk of suffering a stroke from a ruptured brain aneurysm," said study author Daniel Woo, MD, with the University of Cincinnati in Ohio.

The study was supported by the National Institute of Neurological Disorders and Stroke.