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Alzheimer's Disease Press Releases


Fly ‘Nose’ Neurons Help Sniff Out Proteins Suspected of Regulating Neurodegeneration.

Of Mice and Flies: A Cutting-Edge Method for Detecting Neurodegenerative Disease Targets
Thursday, May 16, 2013
Studying neurodegenerative diseases can be like investigating a crime. Scientists inspect damaged nervous tissue, or “the scene”, for suspicious molecules and then work backwards to explain how the suspects may have killed nerve cells. Recently two research groups, one in the United States and the other in the United Kingdom, collaborated to develop a new way to quickly round up many more suspects and test their “alibis”. Their results may lead to more effective treatments for Alzheimer’s disease, Parkinson’s disease and a variety of other neurodegenerative disorders.

Beta-amyloid molecules (green) surround dying neurons (red) in the brains of a new rat model of Alzheimer’s disease.  Courtesy of Town lab, Zilkha Neurogenetic Institute at the University of Southern California Keck School of Medicine.

NIH-funded researchers create next-generation Alzheimer's disease model
Tuesday, Apr 9, 2013
A new genetically engineered lab rat that has the full array of brain changes associated with Alzheimer’s disease supports the idea that increases in a molecule called beta-amyloid in the brain causes the disease, according to a study, published in the Journal of Neuroscience. The study was supported by the National Institutes of Health.

U.S. Army soldier in Afghanistan

First cases of degenerative brain disease CTE found in veterans with blast injuries
Friday, Jun 29, 2012
Some veterans who experience blast-related head injuries can develop the same kind of long-term brain damage seen in athletes who have had multiple head injuries on the playing field. The finding expands the potential public health impact of chronic traumatic encephalopathy (CTE) – the name for degenerative changes in the brain that sometimes occur after a history of multiple concussions.

ApoE4 weakens the blood-brain barrier in mice

NIH-funded research provides new clues on how ApoE4 affects Alzheimer's risk
Wednesday, May 16, 2012
Common variants of the ApoE gene are strongly associated with the risk of developing late-onset Alzheimer's disease, but the gene's role in the disease has been unclear. NIH-funded researchers have found that in mice, the most risky variant of ApoE triggers an inflammatory reaction and damages the blood vessels that feed the brain. An inflammatory molecule called cyclophilin A could be a new target for therapy.

In a mouse model of Alzheimer's disease, the HDAC2 protein is elevated in the hippocampus.

Blockade of learning and memory genes may occur early in Alzheimer's disease
Wednesday, Feb 29, 2012
A repression of gene activity in the brain appears to be an early event affecting people with Alzheimer's disease, researchers funded by the National Institutes of Health have found. In mouse models of Alzheimer's disease, this epigenetic blockade and its effects on memory were treatable.

High blood pressure increases your risk of heart attack and stroke.

NIH study finds stroke risk factors may lead to cognitive problems
Tuesday, Nov 8, 2011
Having common risk factors for stroke can lead to cognitive problems without causing a full-blown stroke. The new findings come from the REGARDS study, an effort to track stroke risk and cognitive health in Americans 45 and older. One of the strongest predictors of cognitive decline was high systolic blood pressure, with each 10 mm Hg increase bumping up the risk by 4 percent.

NINDS small logo

Four new members appointed to National Advisory Neurological Disorders and Stroke Council
Monday, Sep 12, 2011
The NINDS announced that four new members have joined its National Advisory Neurological Disorders and Stroke Council: David M. Holtzman, M.D., David D. Ginty, Ph.D., Paul H. Gross, and Kevin St. P. McNaught, Ph.D. The council serves as the principal advisory body to NINDS regarding the institute’s research program planning and priorities.

A U.S. map showing the Stroke Belt and Buckle in the Southeast

In U.S. Southeast, Cognitive Decline Could Identify Those at High Risk for Stroke
Wednesday, Jul 20, 2011
New research shows that in addition to facing a higher risk of stroke, people living in a part of the Southeastern U.S. known as the Stroke Belt are also at higher risk for cognitive decline as they age. The findings, from the Reasons for Geographic and Racial Differences in Stroke (REGARDS) study, suggest that cognitive decline could be a marker for changes in the brain that increase stroke risk.

Elderly woman

Impaired Clearance, Not Overproduction of Toxic Proteins, May Underlie Alzheimer’s Disease
Thursday, Dec 9, 2010
In Alzheimer’s disease, a protein fragment called beta-amyloid accumulates at abnormally high levels in the brain. Now researchers funded by the National Institutes of Health have found that in the most common, late-onset form of Alzheimer’s disease, beta-amyloid is produced in the brain at a normal rate but is not cleared, or removed from the brain, efficiently.

Photo showing the beta-amyloid that lines the blood vessels of a transgenic Alzheimer's disease mouse. Courtesy of Neuron.

New Evidence that Blood Clots Play a Role in Alzheimer’s Disease
Monday, Oct 4, 2010
Growing evidence points to a connection between Alzheimer’s disease and poor blood flow to the brain. Signs that a stroke has occurred are often found in the brains of Alzheimer’s patients. Meanwhile, there is evidence that stroke and Alzheimer’s disease share similar risk factors, including high blood pressure and atherosclerosis (hardening of the arteries).

Family with Alzheimer's Disease may Carry Clues to Treatment
Wednesday, Jun 17, 2009
In the brains of people with Alzheimer's disease (AD), a toxic protein fragment called beta-amyloid accumulates in clumps that leave a path of damaged brain tissue. Although age is the most powerful risk factor for AD, a small fraction of people develop the disease because of genetic mutations that trigger beta-amyloid accumulation. In a recent study published in Science*, researchers described a family with a mutation that causes beta-amyloid accumulation and AD in some individuals, but could protect against the disease in others.

Huntington’s Disease Protein Affects Nerve Signaling; Study Suggests New Treatments
Thursday, Jun 26, 2008
The abnormal protein found in Huntington’s disease (HD) leads to an unusually large amount of nerve signaling early in the disease process, before other problems appear, a new study shows. Partially blocking these nerve signals prevents neuron death and loss of motor function in fruit flies models of HD. The findings suggest possible new ways of delaying the onset or slowing the progression of the disease.

Reactions to Protein Stress in Neurodegenerative Disease – Sometimes Good, Sometimes Bad and Always Ugly
Friday, Mar 14, 2008
Research has shown that cells have a cleanup system for handling protein "stress," and some studies suggest the possibility of developing therapeutic drugs that would work by giving the system a boost. But a new study published in Neuron suggests that during prolonged stress, the cleanup system can suppress vital cell functions or even actively kill the cell.

New Technique Removes Toxic Protein and Prevents Memory Impairment in Alzheimer's Disease Model
Wednesday, Dec 5, 2007
Increasing the activity of a key protein in the bloodstream slows the buildup of a toxic substance in the brains of mice with the gene mutation for Alzheimer's disease (AD). It also prevents some memory problems, a new study shows. If the approach works in humans, it may eventually lead to a way of preventing or halting AD.

Study Suggests Idebenone May Improve Neurological Function in Friedreich's Ataxia
Wednesday, Dec 5, 2007
Results of a placebo-controlled, double-blind phase II study of the antioxidant idebenone in children with Friedreich's ataxia (FA) suggest that the treatment may lead to improvements in neurological function. It is the first placebo-controlled study to suggest that the neurological deterioration associated with this disease can be slowed or reversed.

A Rollercoaster of Seizure-Like Activity May Damage the Alzheimer's Brain
Tuesday, Nov 27, 2007
Although seizures are not a common symptom of Alzheimer's disease (AD), the brains of people with AD could be humming with seizure-like activity, interrupted by quiet rebound periods that do more harm than good.

Dopamine Drug Leads to New Neurons and Recovery of Function in Rat Model of Parkinson's Disease
Tuesday, Jul 4, 2006
In preliminary results, researchers have shown that a drug which mimics the effects of the nerve-signaling chemical dopamine causes new neurons to develop in the part of the brain where cells are lost in Parkinson's disease (PD). The drug also led to long-lasting recovery of function in an animal model of PD. The findings may lead to new ways of treating PD and other neurodegenerative diseases.

Study Identifies Protein that Impairs Memory in Model for Alzheimer's Disease
Thursday, May 11, 2006
For the first time, researchers have identified a specific form of amyloid beta protein that causes memory impairment long before amyloid plaques and neurodegeneration appear in a mouse model of Alzheimer's disease (AD). The finding may lead to new ways of diagnosing and possibly even preventing the disease.

Study Links Alzheimer's Disease to Abnormal Cell Division
Tuesday, Jan 17, 2006
A new study in mice suggests that Alzheimer's disease (AD) may be triggered when adult neurons try to divide. The finding helps researchers understand what goes wrong in the disease and may lead to new ways of treating it.

Epilepsy Can Be Triggered by Support Cells in the Brain
Thursday, Dec 15, 2005
For decades, researchers have tried to understand what triggers clusters of neurons to begin signaling excessively in epilepsy. A new study shows that, in many cases, the answer resides in star-shaped support cells called astrocytes. The finding may lead to new ways of treating epilepsy.

Study Links Progressive Aphasia Syndrome to Prion Gene
Monday, Nov 28, 2005
Most people with a rare type of dementia called primary progressive aphasia (PPA) have a specific combination of prion gene variants, a new study shows. The study is the first to link the prion protein gene to this disorder. The researchers also looked at the prion protein gene in people with Alzheimer's disease and amyotrophic lateral sclerosis (ALS or Lou Gehrig's disease) and did not find any association with specific gene variants in those disorders.

Study Identifies New Mode of Action for Ataxia Gene
Wednesday, Oct 19, 2005
For the first time, researchers have identified how the gene for a hereditary neurodegenerative disease called spinocerebellar ataxia type 1 (SCA1) disables an important group of neurons in the brain. The findings improve understanding of how SCA1 and related diseases develop and may lead to new ways of treating them.

Drug Screening Study Suggests New Treatments for Alzheimer's
Monday, Sep 26, 2005
While several treatments are currently available for Alzheimer's disease (AD), none of them can slow or halt the course of this devastating disorder. In a new study, researchers have now identified three compounds that inhibit an enzyme believed to be involved in the process that leads to AD. This discovery may lead to new treatments that can stop the disease process in its tracks.

What's Old is New Again - Antibiotic Protects Nerves By Removing Excess Glutamate
Monday, Feb 7, 2005
A new study shows that a common antibiotic used to treat bacterial infections increases survival rates and delays nerve damage in a mouse model for amyotrophic lateral sclerosis (ALS). The antibiotic works by activating or "turning on" the gene encoding the glutamate transporter in neurons. This finding may lead to new drug treatments for ALS and other neurodegenerative diseases.

Study Using Robotic Microscope Shows How Mutant Huntington's Disease Protein Affects Neurons
Wednesday, Oct 13, 2004
Using a specially designed robotic microscope to study cultured cells, researchers have found evidence that abnormal protein clumps called inclusion bodies in neurons from people with Huntington's disease (HD) prevent cell death. The finding helps to resolve a longstanding debate about the role of these inclusion bodies in HD and other disorders and may help investigators find effective treatments for these diseases.
Fact Sheet

Vaccine Reduces Parkinson's Disease Neurodegeneration in Mice
Wednesday, Jul 28, 2004
For the first time, researchers have shown that an experimental vaccine can reduce the amount of neurodegeneration in a mouse model for Parkinson's disease. The finding suggests that a similar therapy might eventually be able to slow the devastating course of Parkinson's disease in humans.
Fact Sheet

Yeast Model Yields Insight into Parkinson's Disease
Thursday, Dec 4, 2003
Scientists who developed the first yeast model of Parkinson's disease (PD) have been able to describe the mechanisms of an important gene's role in the disease. Tiago Fleming Outeiro, Ph.D., and Susan Lindquist, Ph.D., of the Whitehead Institute for Biomedical Research in Cambridge, Massachusetts, studied the gene's actions under normal conditions and under abnormal conditions to learn how and when the gene's product, alpha-synuclein, becomes harmful to surrounding cells. The scientists created a yeast model that expresses the alpha-synuclein gene, which has been implicated in PD. Yeast models are often used in the study of genetic diseases because they offer researchers a simple system that allows them to clarify how genes work.
Fact Sheet

Major New Finding on Genetics of Parkinson's Disease Zeroes In on Activity of Alpha Synuclein
Thursday, Oct 30, 2003
Scientists investigating a rare familial form of early-onset Parkinson's disease have discovered that too much of a normal form of the alpha-synuclein gene may cause Parkinson's disease. The finding, reported in the October 31, 2003, issue of Science, shows that abnormal multiplication of the alpha-synuclein gene can cause the disease.
Fact Sheet

Misbehaving Molecules: 3-Dimensional Pictures of ALS Mutant Proteins Support Two Major Theories About How the Disease is Caused
Sunday, May 18, 2003
A new study reveals for the first time how gene mutations lead to the inherited form of amyotrophic lateral sclerosis (ALS), or Lou Gehrig's disease. The study suggests that the two most prominent theories of how familial ALS (FALS) and other related diseases develop are both right in part.
Fact Sheet

What's in a Connection? A Look at Protein Patterns Within Synapses
Monday, May 5, 2003
A new study has begun to unravel the mysteries of protein interactions that govern the strength of nerve cell connections, or synapses, in the brain. The findings give researchers a better understanding of how synapses function during learning and memory, and they may lead to new insights about such neurological disorders as Parkinson's and Alzheimer's diseases.

Researchers Find Genetic Links for Late-Onset Parkinson's Disease
Wednesday, Dec 19, 2001
Recent studies provide strong evidence that genetic factors influence susceptibility to the common, late-onset form of Parkinson's disease (PD). The findings improve scientists' understanding of how PD develops and may lead to new treatments or even ways of preventing the disease.
Fact Sheet

NINDS Hosts First Parkinson's Disease Implementation Committee Meeting to Establish Priorities for Parkinson's Research
Monday, Jul 31, 2000
The first meeting of the NINDS Parkinson's Disease Implementation Committee (PDIC) was held July 31, 2000 at the National Institutes of Health, Neuroscience Center in Rockville, Maryland. The Committee identified several areas of Parkinson's disease research that will receive the highest priority in the coming weeks, including clinical trials and gene research.

NINDS Funds Five Specialized Neuroscience Programs at Minority Institutions
Tuesday, Jan 18, 2000
The National Institute of Neurological Disorders and Stroke (NINDS), in collaboration with the National Center for Research Resources (NCRR) and the Office for Research on Minority Health (ORMH), recently awarded grants to five minority institutions under a new funding mechanism called Specialized Neuroscience Research Programs at Minority Institutions (SNRP).

Transplanted Neural Stem Cells Migrate Throughout the Abnormal Brain, Reduce Disease Symptoms
Monday, Jun 7, 1999
For years, researchers have probed the mysteries of neural stem cells -- immature cells that can differentiate into all the cell types that make up the brain -- with the idea that they might be useful for treating brain disorders such as Parkinson's disease. Important new animal research now suggests that these cells may be effective in treating a much broader array of brain diseases than previously anticipated, including Alzheimer's disease and many childhood brain disorders.

Long-Time NIH Grantee Stanley B. Prusiner Wins Nobel Prize
Monday, Oct 6, 1997
Stanley B. Prusiner, M.D., a long-time grantee of the National Institutes of Health (NIH), is the recipient of the 1997 Nobel Prize in physiology or medicine for his discovery of an unusual class of infectious particles called prions. Prions are believed to be responsible for a group of diseases that include "mad cow" disease. Prusiner, who is professor of neurology, virology, and biochemistry at the University of California, San Francisco (UCSF), has received more than 56 million dollars in research grant support from NIH during the last three decades.

Protein Marker Found in Transmissible Spongiform Encephalopathies: Finding May Lead to Diagnostic Test for Human, Cattle Disorders
Wednesday, Sep 25, 1996
A protein widely distributed in tissues throughout the body, with the highest concentration in the brain, has been shown to be a specific marker in the spinal fluid of humans and animals infected with transmissible spongiform encephalopathies, scientists say. This discovery paves the way for the development of an improved test for the diagnosis of Creutzfeldt-Jakob disease in humans and encephalopathies in animals. The test could enable precise identification of disease in British cattle presently targeted for slaughter because of suspected infection with bovine spongiform encephalopathy, known as Mad Cow disease.

Clues found for early memory loss in Alzheimer's disease
Thursday, Apr 7, 1994
Scientists at the National Institute of Neurological Disorders and Stroke (NINDS) have discovered that adding a substance called beta amyloid to normal skin cells causes the cells to exhibit the same type of molecular dysfunction previously demonstrated in skin cells of patients with Alzheimer's disease (AD). This step may lead to a new explanation of memory loss, one of the earliest and most common symptoms of the disease.

Discovery may lead to skin tests for Alzheimer's disease; Finding could also point to underlying cause of the disorder
Tuesday, Aug 31, 1993
Scientists at the National Institute of Neurological Disorders and Stroke (NINDS) in Bethesda, MD, and the Burke Medical Research Institute at Cornell Medical College in White Plains, NY, have discovered physiological differences in the skin cells of those with Alzheimer's disease (AD), a finding that could lead to a standard battery of skin tests for diagnosing the disease.

NINDS Hails Discovery of Gene for Familial ALS
Wednesday, Mar 3, 1993
Officials at the National Institute of Neurological Disorders and Stroke (NINDS) hailed the identification of a gene associated with the familial form of ALS (Lou Gehrig's disease). "This discovery is extremely important because it marks the first identification of a specific gene for a neurodegenerative disease of adult life," said Carl M. Leventhal, M.D., director of the NINDS program that contributed to support for the research reported in the March 3 issue of Nature*. "It also suggests a likely mechanism for the damage to nerve cells in familial ALS and, possibly, other brain disorders."

NINDS Scientists Isolate Segments Of DNA Sequence That Identify More Than 2,300 Brain Genes
Wednesday, Feb 12, 1992
Using a novel strategy, scientists from the National Institute of Neurological Disorders and Stroke have isolated segments of DNA sequence that uniquely identify more than 2,300 brain genes. The recent data, combined with data from 347 segments sequenced earlier by NINDS scientists, doubles the total number of human genes identified by sequencing, scientists report in the February 13 issue of Nature.

NINDS Scientists Develop Strategy To Speed Gene and Brain Research
Thursday, Jun 20, 1991
Using a novel strategy, scientists at the National Institute of Neurological Disorders and Stroke (NINDS) have isolated key identifying regions of more than 400 genes that work inside the human brain. The scientists say their work should help identify genetic defects that cause brain disease and speed progress of genetics research.

Creutzfeldt-Jakob Gene Mutation Found
Thursday, Aug 30, 1990
Scientists at the National Institute of Neurological Disorders and Stroke (NINDS) have linked three outbreaks of Creutzfeldt-Jakob disease (CJD) in Europe and Israel to a genetic mutation found in the outbreaks' victims.