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NYU Langone Medical Center's tip sheet to the International Conference on Alzheimer's Disease 2008
Date:7/25/2008

NEW YORK, July 26, 2008 NYU Langone Medical Center researchers have long been making important contributions to the understanding of Alzheimer's disease. They were among the first to characterize amyloid, the plaque-forming protein implicated in Alzheimer's, and the first to describe a genetic mutation in a familial form of the disease. They also developed the first successful intervention program to reduce the need for placing patients in nursing homes and alleviate caregivers' depression.

At the 2008 ICAD meeting, NYU Langone Medical Center researchers are presenting a wide range of findings from both clinical studies using state-of-the-art methods to discern the earliest sign of Alzheimer's and from animal studies aimed at understanding how amyloid causes neuronal dysfunction in the brain. All of this research helps advance the understanding of Alzheimer's, which now afflicts more than 5 million Americans. A better understanding, it is hoped, will lead to more effective therapies that will slow the progression of the disease and ultimately to ways to prevent its onset.

The following news tips are based on poster and oral presentations at the Alzheimer's Association 2008 International Conference to be held in Chicago from July 26 to July 31. Each presentation is embargoed for a specific date and time.

Brain Atrophy and Biomarkers May Help Identify People at Risk for Alzheimer's
Susan de Santi, Ph.D., Associate Professor, Department of Psychiatry, NYU Langone Medical Center
EMBARGOED FOR RELEASE UNTIL TUESDAY, July 29, 2008 at 12:30 p.m. CT

By combining MRI brain scans and measurements of certain compounds in the cerebrospinal fluid, NYU researchers were able to distinguish individuals who would develop Alzheimer's disease over a two-year period. In a study of 23 people, they found atrophy in areas of the brain involved in learning and memory, and significantly higher CSF levels of phosphorylated tau and other compounds among individuals who would develop Alzheimer's compared to those individuals who didn't progress from mild cognitive impairment over the two-year period. This preliminary study suggests that combining these tests could help predict which individuals with mild cognitive impairment are at the highest risk for developing Alzheimer's disease.
Presentation # P3-067


Big Immune Response to Common Mouth Bacteria Linked to Alzheimer's.
Angela R Kamer, D.M.D., M.S., PhD., Assistant Professor, College of Dentistry, New York University
EMBARGOED FOR RELEASE UNTIL SUNDAY, July 27, 2008, at 12:30 p.m. CT

In a study investigating the link between Alzheimer's disease and a heightened inflammatory-immune response, NYU researchers found that twice as many subjects with probable Alzheimer's disease tested positive for antibodies in their plasma against a type of bacteria that is commonly found in the mouth. The pioneering study supports a growing body of evidence that associates notable immune changes with a means of predicting and classifying Alzheimer's disease. Together with other immune markers associated with Alzheimer's disease, antibodies to these periodontal bacteria could serve to better understand the causes and mechanisms of the disease, the researchers say.
Presentation # P1-348


Signs of Brain Disease among Healthy Individuals
Lidia Glodzik, MD, PhD, Research Physician, Center for Brain Health at NYU Langone Medical Center
EMBARGOED FOR RELEASE UNTIL TUESDAY, July 29, 2008 at 12:30 p.m. CT

NYU researchers identified signs of pathology before the clinically noticeable stages of mild cognitive impairment that normally precede Alzheimer's disease. The study involved a cognitively normal group of people ages 40 to 86. It found that higher levels of tau protein in the cerebrospinal fluid correlated with lower grey matter density in brain regions that are important for learning and memory, and are susceptible to Alzheimer's. Combining cerebrospinal fluid measurements and imaging markers to identify normal subjects who are more vulnerable to the neurodegenerative disease opens an opportunity to explore early detection in the service of prevention, the researchers report.
Presentation # PS-070


Couples Counseling Helps the Spouse Caregiver
Mary S. Mittelman, Dr.P.H., Research Professor in the Department of Psychiatry at New York University School of Medicine
EMBARGOED FOR RELEASE UNTIL WEDNESDAY July 30 at 2:30 p.m. CT

When the patient with Alzheimer's and their spouse caregiver are counseled separately, they are expected to go home and live together. Can couples counseling help stabilize their relationship as they grapple with the disease? Early results show that it can. In a pilot study, researchers at NYU's Silberstein Center offered six counseling sessions focused on the new needs of each member of a couple brought about by the illness. Each of the ill spouses was in the early stages of dementia and could still participate in a counseling session. The NYU researchers report that all caregivers were surprised by how much the person with dementia could communicate in the session. They also report that relationships improved as a result of the counseling, and the caregivers became less depressed.
Presentation # P4-429


Subjective Memory Complaints a Predictor of Further Cognitive Decline
Barry Reisberg, MD, Professor, Department of Psychiatry at NYU Langone Medical Center
EMBARGOED FOR RELEASE UNTIL TUESDAY, July 29, 2008 at 12:30 p.m. CT

An NYU study that followed 213 healthy adults over an average of 7 years found that subjects with subjective memory complaints at the first evaluation were almost 7 times more likely to experience cognitive decline to mild cognitive impairment or dementia compared to adults without initial complaints. This is the first prediction study to link subjective cognitive impairment to both mild cognitive impairment and dementia and underlines the importance in studying early, non-specific symptoms that arise before mild cognitive impairment is apparent, the researchers report. Such efforts are critical to preventing the disease. To develop preventive interventions it may be necessary to accurately identify the disease in its earliest manifestations, when symptoms are first emerging, say the NYU researchers. These subjective symptoms appear to occur as early as twenty or more years before the overt dementia of Alzheimer's appears.
Presentation # PS-043


A Decreasing Ability to Learn Among Aging Healthy Carriers of APOE 4
Nunzio Pomara, M.D., Professor in the Department of Psychiatry, NYU Langone Medical Center; Director of the Geriatric Psychiatry Program, Nathan S. Kline Institute
EMBARGOED FOR RELEASE WEDNESDAY, July 30, 2008, at 1 PM CT

A new study by NYU researchers at the Nathan Kline Institute suggests that a major genetic risk factor for Alzheimer's disease, apoE 4, may exert its adverse effects long before clinical symptoms of the disease emerge. During this critical period they believe there may be a gradually decreasing ability to learn new material, and subsequently form new memories. The scientists evaluated 184 healthy adults, ages 38 to 80 (64 people carried the apoE4 allele), using standardized measures of verbal learning and memory, such as learning a list of words. At younger ages, surprisingly, those with the apoE 4 genetic risk factor significantly outperformed those without it. By ages 60 to 64 and older, however, performance in the apoE 4 group dropped below the non-apoE 4 group.
Presentation # HT-3577


Genetic Mutation Linked to a More Abundant Form of Alzheimer's Protein
Allal Boutajangout, PhD, Research Assistant Professor, Department of Medicine and Psychiatry at NYU Langone Medical Center
EMBARGOED FOR RELEASE UNTIL WEDNESDAY July 30, 2008 at 4:00 p.m. CT

NYU researchers found that a specific gene mutation previously associated with an increase in production of an Alzheimer's disease-causing protein, amyloid beta, also promotes the entanglement of another protein, tau, which also is associated with the neurodegenerative disease. Mice that produced human types of tau while expressing the gene mutation showed a significant increase in the harmful form of the tau protein in the brain. The research provides a new model for Alzheimer's onset and progression.
Presentation #04-01-05


Study Further Ties Digestion of Harmful Protein to Alzheimer's Disease
Dun-Sheng Yang, PhD, Assistant Professor, Department of Psychiatry, NYU Langone Medical Center; Research Scientist, Center for Dementia Research, Nathan S. Kline Institute
EMBARGOED FOR RELEASE UNTIL SUNDAY, July 27, 2008 at 12:30 p.m. CT

NYU researchers genetically enhanced the activity of digestive enzymes in the nerve cells of mice that were susceptible to producing an overabundant amount of amyloid beta, the abnormal protein found in the plaques littering the brains of people with Alzheimer's. The mice showed lower amounts of the protein in parts of the brain responsible for advanced thinking, learning and memoryevidence that their brain cells were more efficient at digesting and expelling the toxic, misfolded protein, the researchers report. The study shows that the failure to degrade amyloid beta in lysosomes containing the digestive enzymes is an important factor in Alzheimer's disease. Amyloid beta and another protein called tau are associated with the disease, but it hasn't yet been proven definitively that either actually causes the disease.
Presentation # P1-059


Study Suggests a Link Between Amyloid and Memory
Paul M. Mathews, PhD, Assistant Professor, Department of Psychiatry, NYU Langone Medical Center; Research Scientist, Center for Dementia Research, Nathan S. Kline Institute
EMBARGOED FOR RELEASE UNTIL SUNDAY, JULY 28, 2008 at 3:00 p.m. CT

By manipulating levels of the beta amyloid peptide, which accumulates in brain plaques in people with Alzheimer's disease, NYU researchers have found that the peptide not only plays a toxic role in the neurodegenerative disease but also is crucial in modulating learning and memory consolidation in the normal brain. The rat study, which controlled peptide levels in a region of the brain that is important in learning and memory, suggests that its disruption may be one of the underlying causes of nerve dysfunction during Alzheimer's disease pathogenesis.
Presentation #02-02-01


Dysfunctional Transporters in Nerves Related to Alzheimer's
Seonil Kim, Ph.D student, Sackler Institute for Graduate Biomedical Sciences, NYU Langone Medical Center, Graduate Training Program in Cellular and Molecular Biology, Nathan S. Kline Institute and Ralph Nixon, M.D., Ph.D., Professor of Psychiatry and Cell Biology, NYU Langone Medical Center
EMBARGOED FOR RELEASE UNTIL TUESDAY, JULY 29, 2008 at 12:30 p.m. CT

An NYU study found that membrane vesicles that are essential for the trafficking of materials across nerve cells are an important factor in the pathology of Alzheimer's disease. Mouse neurons which over-produce a precursor to the amyloid protein closely linked to Alzheimer's disease development were unable to shuttle the vesicles to their proper destinations in nerve cells, causing them instead to enlarge abnormally and accumulate. The impeded transport of these vesicles, according to the researchers, may affect communications within and between nerve cells that are critical for cognition and when disrupted can lead to the neurodegeneration of Alzheimer's disease.
Presentation # PS-410


Early Phases of Creating a Vaccine against Prion Disease
Thomas Wisniewski, MD, Department of Pathology at NYU Langone Medical Center
EMBARGOED FOR RELEASE UNTIL TUESDAY, July 29, 2008 at 11:30 a.m. CT

In an animal study, NYU researchers bolstered immunity against a toxic and infectious version of the prion protein, which causes a group of brain diseases, including mad cow's disease. By injecting a safe, reconfigured form of the protein into the body cavity of mice, in addition to orally delivering a neutral bacterial booster, animals could produce more antibodies against the prion protein in the mouth and blood system, preventing access of the infectious prions to the brain. The inoculated mice remained symptom free for 400 days after exposure to infectious prion, while their brains were free from the disease causing protein. The finding has the potential to safely curb prion diseases, such as chronic wasting disease and variant Creutzfeld-Jacob disease, which are thought to be spread by oral exposure to prion.
Presentation # S3-01-04


Tau Immunotherapy Prevents Cognitive Decline in an Alzheimer's Mouse Model
Einar M. Sigurdsson, PhD, Assistant Professor of Psychiatry and Pathology, NYU Langone Medical Center
EMBARGOED FOR RELEASE UNTIL WEDNESDAY, JULY 30, 2008 at 3:45 p.m. CT

NYU researchers have successfully prevented the cognitive decline of mice by employing a vaccine that targets tangles of tau, a type of protein associated with Alzheimer's disease. Tests confirmed that the immunotherapy helped preserve cognition as well as reduced tau protein tangles in the brain. The findings support the possibility of an immunotherapy that treats Alzheimer's disease by directly targeting toxic forms of the tau protein.
Presentation # O4-04-04


Enzyme inhibition modulates Alzheimer's pathology in mice
Jose Morales-Corraliza, Ph.D, NYU Langone Medical Center and Research Scientist, Nathan S. Kline Institute
EMBARGOED FOR RELEASE UNTIL SUNDAY, JULY 27, 2008 at 12:30 p.m. CT Researchers at NYU Langone Medical Center and the Nathan Kline Institute found that the inhibition of the calpain enzyme, which is involved in various cellular processes, led to a robust decrease in amyloid deposition in mice that develop plaque pathology commonly seen in Alzheimer's disease. Modulation of neuronal calpain activity presents a potential therapeutic approach to Alzheimer's, they report.
Presentation #P1-079


Partial gene-deletion improves memory dysfunction in Alzheimer's mice
Masuo Ohno, Ph.D., NYU Langone Medical Center and head of the Laboratory of Molecular and Cellular Cognition, Center for Dementia Research at the Nathan Kline Institute
EMBARGOED FOR RELEASE UNTIL SUNDAY, JULY 27, 2008 at 12:30 p.m. CT

An animal study by NYU researchers reveals that partially inhibiting an enzyme that initiates the release of amyloid beta led to an improvement in neuronal and cognitive deficits in mice that produced excessive amounts of the plaque forming protein. The approach poses a possibility to rescue Alzheimer's-related deficits, the researchers report.
Presentation #P1-092


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Contact: Bob Brody
bobbrody@hotmail.com
212-404-3555
NYU Langone Medical Center / New York University School of Medicine
Source:Eurekalert

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