Alzheimer's Disease Press Releases
New NIH-funded memory drug moves into Phase 1 clinical study
Thursday, Dec 31, 2015
An experimental drug that may improve memory is now being tested in a Phase 1 safety trial. The compound, BPN14770, was developed by Tetra Discovery Partners, with support from the NIH Blueprint Neurotherapeutics Network, a program designed to facilitate the discovery and development of novel neurological treatments. It is the first compound funded by the program to reach a Phase 1 clinical trial.
Speeding up brain’s waste disposal may slow down neurodegenerative diseases
Monday, Dec 21, 2015
A study of mice shows how proteasomes, a cell’s waste disposal system, may break down during Alzheimer’s disease (AD), creating a cycle in which increased levels of damaged proteins become toxic, clog proteasomes, and kill neurons. The study, published in Nature Medicine and supported by the National Institutes of Health, suggests that enhancing proteasome activity with drugs during the early stages of AD may prevent dementia and reduce damage to the brain.
DNA repair factor linked to breast cancer may also play a role in Alzheimer’s disease
Monday, Nov 30, 2015
Mutant forms of breast cancer factor 1 (BRCA1) are associated with breast and ovarian cancers but according to new findings, in the brain the normal BRCA1 gene product may also be linked to Alzheimer’s disease. The results, published in Nature Communications, suggest that low levels of BRCA1 protein in the brain may contribute to dementia. The study was funded by the National Institutes of Health.
Nuclear transport problems linked to ALS and FTD
Friday, Oct 16, 2015
Three teams of scientists supported by the National Institutes of Health showed that a genetic mutation linked to some forms of amyotrophic lateral sclerosis (ALS) and frontotemporal degeneration (FTD) may destroy neurons by disrupting the movement of materials in and out of the cell’s nucleus, or command center where most of its DNA is stored.
Dormant viral genes may awaken to cause ALS
Wednesday, Sep 30, 2015
Scientists at the National Institutes of Health (NIH) discovered that reactivation of ancient viral genes embedded in the human genome may cause the destruction of neurons in some forms of amyotrophic lateral sclerosis (ALS).
Scientists uncover nuclear process in the brain that may affect disease
Monday, Aug 17, 2015
Every brain cell has a nucleus, or a central command station. Scientists have shown that the passage of molecules through the nucleus of a star-shaped cell, called an astrocyte, may play a critical role in health and disease. The study, published in the journal Nature Neuroscience, was partially funded by the National Institutes of Health (NIH).
Scientists create mice with a major genetic cause of ALS and FTD
Friday, May 22, 2015
Scientists at Mayo Clinic, Jacksonville, Florida created a novel mouse that exhibits the symptoms and neurodegeneration associated with the most common genetic forms of frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS, Lou Gehrig’s disease), both of which are caused by a mutation in the a gene called C9ORF72.
Study reveals how genetic changes lead to familial Alzheimer’s disease
Wednesday, Mar 11, 2015
Mutations in the presenilin-1 gene are the most common cause of inherited, early-onset forms of Alzheimer’s disease. In a new study, published in Neuron, scientists replaced the normal mouse presenilin-1 gene with Alzheimer’s-causing forms of the human gene to discover how these genetic changes may lead to the disorder.
New members selected for National Advisory Neurological Disorders and Stroke Council
Thursday, Jan 29, 2015
Five prominent individuals from the neuroscience community have joined the National Advisory Neurological Disorders and Stroke Council, the principal advisory body to the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health.
NIH announces grants for frontotemporal degeneration research
Thursday, Oct 23, 2014
The National Institutes of Health will award three large, five-year projects on a specific form of dementia, known as frontotemporal because of the areas of the brain that are affected. The projects, funded by the NIH’s National Institute of Neurological Disorders and Stroke (NINDS), National Institute on Aging (NIA) and the National Center for Advancing Translational Sciences (NCATS), announced today total more than $5.9 million for 2014.
Scientists sniff out unexpected role for stem cells in the brain
Friday, Oct 10, 2014
For decades, scientists thought that neurons in the brain were born only during the early development period and could not be replenished. More recently, however, they discovered cells with the ability to divide and turn into new neurons in specific brain regions.
NIH scientists find six new genetic risk factors for Parkinson’s
Sunday, Jul 27, 2014
A new international study has taken number crunching to the extreme. Using data from over 18,000 patients, scientists identified more than two dozen genetic risk factors involved in Parkinson’s disease, including six that had not been previously reported. The study, published in Nature Genetics, was partially funded by the National Institutes of Health (NIH) and led by scientists working in NIH laboratories.
NIH scientists take totally tubular journey through brain cells
Wednesday, Jun 11, 2014
In a new study, scientists at the National Institutes of Health took a molecular-level journey into microtubules, the hollow cylinders inside brain cells that act as skeletons and internal highways. They watched how a protein called tubulin acetyltransferase (TAT) labels the inside of microtubules. The results, published in Cell, answer long-standing questions about how TAT tagging works and offer clues as to why it is important for brain health.
Shining a light on memory
Sunday, Jun 1, 2014
Using a flash of light, scientists have inactivated and then reactivated a memory in genetically engineered rats. The study, supported by the National Institutes of Health, is the first cause-and-effect evidence that strengthened connections between neurons are the stuff of memory.
Longevity gene may boost brain power
Friday, May 9, 2014
Scientists showed that people who have a variant of a longevity gene, called KLOTHO, have improved brain skills such as thinking, learning and memory regardless of their age, sex, or whether they have a genetic risk factor for Alzheimer’s disease. Increasing KLOTHO gene levels in mice made them smarter, possibly by increasing the strength of connections between nerve cells in the brain.
3-D changes in DNA may lead to a genetic form of Lou Gehrig’s disease
Wednesday, Mar 5, 2014
New findings reveal how a mutation, a change in the genetic code that causes neurodegeneration, alters the shape of DNA, making cells more vulnerable to stress and more likely to die.
NIH and NFL tackle concussion research
Monday, Dec 16, 2013
The National Institutes of Health has selected eight projects to receive support to answer some of the most fundamental problems on traumatic brain injury, including understanding long-term effects of repeated head injuries and improving diagnosis of concussions.
Study breaks blood-brain barriers to understanding Alzheimer’s
Friday, Dec 13, 2013
Researchers used mice to show how a breakdown of the brain’s blood vessels may amplify or cause problems associated with Alzheimer’s disease. The results published in Nature Communications suggest that blood vessel cells, called pericytes, may provide novel targets for treatments and diagnoses.
Brain may flush out toxins during sleep
Thursday, Oct 17, 2013
A good night’s rest may literally clear the mind. Using mice, researchers showed for the first time that the space between brain cells may increase during sleep, allowing the brain to flush out toxic neurodegenerative molecules that build up during waking hours. These results suggest a new role for sleep in health and disease. The study was funded by the National Institute of Neurological Disorders and Stroke (NINDS), part of the NIH.
NIH researchers discover how brain cells change their tune
Thursday, Jul 25, 2013
Brain cells talk to each other in a variety of tones. Sometimes they speak loudly but other times struggle to be heard. For many years scientists have asked why and how brain cells change tones so frequently. Today National Institutes of Health researchers showed that brief bursts of chemical energy coming from rapidly moving power plants, called mitochondria, may tune brain cell communication.
Altered protein shapes may explain differences in some brain diseases
Wednesday, Jul 3, 2013
It only takes one bad apple to spoil the bunch, and the same may be true of certain proteins in the brain. Studies have suggested that just one rogue protein (in this case, a protein that is misfolded or shaped the wrong way) can act as a seed, leading to the misfolding of nearby proteins. According to an NIH-funded study, various forms of these seeds — originating from the same protein — may lead to different patterns of misfolding that result in neurological disorders with unique sets of symptoms.
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.
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.
Breaking News from Society for Neuroscience 2012
Wednesday, Oct 17, 2012
Hundreds of NIH-funded studies are being presented at the 2012 Society for Neuroscience annual meeting. Here, the National Institute of Neurological Disorders and Stroke has highlighted a selection of studies and events led by our grantees.
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.
NIH-supported study shows how immune cells change wiring of the developing mouse brain
Wednesday, May 23, 2012
Researchers have shown in mice how immune cells in the brain target and remove unused connections between brain cells during normal development. This research, supported by the National Institutes of Health, sheds light on how brain activity influences brain development, and highlights the newly found importance of the immune system in how the brain is wired, as well as how the brain forms new connections throughout life in response to change.
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.
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.
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.
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.
NIH database will speed research toward better prevention, diagnosis and treatment of TBI
Monday, Aug 29, 2011
NIH, in partnership with the Department of Defense, is building the Federal Interagency Traumatic Brain Injury Research (FITBIR) database. The database is expected to accelerate research toward better treatment and diagnosis of TBI by making it easier to compare results across studies.
NIH Blueprint empowers drug development for nervous system disorders
Thursday, Aug 18, 2011
The NIH Blueprint for Neuroscience Research has made awards to investigators across the United States for an ambitious set of projects seeking to develop new drugs for disorders of the nervous system. The projects are part of the NIH Blueprint Neurotherapeutics Network, which will be funded at up to $50 million over the next five years.
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.
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.
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).
Four New Members Appointed to National Neurological Disorders and Stroke Advisory Council
Thursday, Feb 4, 2010
Four New Members Appointed to National Neurological Disorders and Stroke Advisory Council
Dr. William Matthew Tapped to Lead NINDS Office of Translational Research
Thursday, Jul 30, 2009
The National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health, has named William D. Matthew, Ph.D., as director of its Office of Translational Research (OTR).
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.
Immune Cells Protect Against Alzheimer’s Disease
Wednesday, May 9, 2007
Immune cells in the brain help slow the accumulation of beta-amyloid that is a hallmark of Alzheimer’s disease (AD), a new study shows. The researchers also found that a specific immune system protein strongly affects mortality in a mouse model of AD.
In Brain, One Gene is Worth a Thousand Words
Tuesday, Feb 20, 2007
Using microarray technology, researchers supported by the National Institutes of Health (NIH) have shown that people with one variant of a gene that’s active in the brain have better episodic memory – the ability to remember events and facts – than do people without that variant. The researchers are using the same technology to identify genetic risk factors associated with neurological diseases.
Developing Tools to Detect Cognitive Impairment from Silent Strokes
Monday, Nov 6, 2006
Scientists from the National Institute of Neurological Disorders and Stroke (NINDS) and the Canadian Stroke Network recently wrapped up a workshop – the first of its kind – aimed at harmonizing clinical and research tools for assessing vascular cognitive impairment (VCI), a common disability linked to stroke.
Enzyme Reverses Memory Loss in Alzheimer’s Mouse Model
Monday, Nov 6, 2006
Increasing the amount of a specific enzyme in the brain partially restores memory in a mouse model for Alzheimer’s disease (AD), researchers say. The results could eventually lead to new treatments for AD or other neurodegenerative disorders.
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 Implicates Potassium Channel Mutations in Neurodegeneration and Mental Retardation
Sunday, Feb 26, 2006
For the first time, researchers have linked mutations in a gene that regulates how potassium enters cells to a neurodegenerative disease and to another disorder that causes mental retardation and coordination problems. The findings may lead to new ways of treating a broad range of disorders, including Alzheimer's and Parkinson's diseases. The study was funded in part by the National Institutes of Health's National Institute of Neurological Disorders and Stroke (NINDS).
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.
Toxic Interactions from Neighboring Cells May Be Necessary for Huntington’s disease
Tuesday, Sep 27, 2005
A new study suggests that interactions between different cells are critical for the development of Huntington’s disease (HD) and perhaps other neurodegenerative diseases. This study provides the first genetic evidence that cell-cell interactions may be a necessary step in the onset of HD symptoms in a mouse model. This knowledge may lead to new therapeutic strategies to treat HD.
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.
Statins Prevent a "Sticky" Situation in the Formation of Plaques
Wednesday, Mar 9, 2005
Studies have suggested that statins, a class of cholesterol-lowering drugs, may also lower the risk for Alzheimer’s disease (AD). A new study now suggests that some of the beneficial effects of the drug may be derived from a cholesterol-independent activity. This research, performed in mouse cells carrying an AD-causing gene mutation, may help scientists understand the clinical benefits of statins in AD.
Test Could Improve Detection of Prion Disease in Humans
Monday, Feb 14, 2005
A highly sensitive post-mortem test could help scientists more accurately determine if a person died of Creutzfeldt-Jakob disease (CJD), a human neurological disorder caused by the same class of infectious proteins that trigger mad cow disease, according to a new study supported in part by the National Institutes of Health (NIH). The finding opens the possibility that such testing might be refined in the future so it can be used to detect prion disease in living people and animals before the onset of symptoms.
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.
Anti-Cholesterol Drug May Block Amyloid Pathology in Alzheimer’s Disease
Friday, Jan 14, 2005
A drug designed to inhibit cholesterol production may also block the production of amyloid, a hallmark of Alzheimer’s disease (AD). In a mouse model of the disease, the drug reduced amyloid buildup by up to 99 percent and worked for up to 2 months without any evidence of toxicity.
Study Using Robotic Microscope Shows How Mutant Huntington's Disease Protein Affects Neurons
Wednesday, Oct 13, 2004
Vaccine Reduces Parkinson's Disease Neurodegeneration in Mice
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.
Wednesday, Jul 28, 2004
Yeast Model Yields Insight into Parkinson's Disease
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.
Thursday, Dec 4, 2003
Major New Finding on Genetics of Parkinson's Disease Zeroes In on Activity of Alpha Synuclein
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.
Thursday, Oct 30, 2003
Investigators Explore Selective Silencing of Disease Genes
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.
Wednesday, Oct 15, 2003
Study Links Restless Legs Syndrome to Poor Iron Uptake in the Brain
A new strategy to shut down mutant gene expression in the brain may someday be useful to treat a wide range of hereditary neurodegenerative diseases, such as Huntington’s, Alzheimer’s, and Parkinson’s diseases.
Monday, Aug 11, 2003
Misbehaving Molecules: 3-Dimensional Pictures of ALS Mutant Proteins Support Two Major Theories About How the Disease is Caused
Results of the first-ever autopsy study of brains from people with restless legs syndrome (RLS) suggest that the disorder may result from inefficient processing of iron in certain brain cells. The findings provide a possible explanation for this disorder and may lead to new ways of treating the disease.
Sunday, May 18, 2003
What's in a Connection? A Look at Protein Patterns Within Synapses
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.
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.
Dystonia Protein Linked to Problem Common in Other Neurological Disorders
Monday, Mar 24, 2003
Researchers Find Genetic Links for Late-Onset Parkinson's Disease
A new study links the protein that is impaired in the movement disorder torsion dystonia to a problem that is common to many neurological diseases. The finding may point to new treatments for dystonia, Parkinson's disease, and other disorders.
Wednesday, Dec 19, 2001
NINDS Hosts First Parkinson's Disease Implementation Committee Meeting to Establish Priorities for Parkinson's Research
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.
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.
NINDS Awards Almost $24 Million to Support Parkinson's Disease Research Centers of Excellence
Friday, Dec 4, 1998
Three top university hospitals will receive a total of almost $24 million from the National Institute of Neurological Disorders and Stroke (NINDS) to advance understanding of Parkinson's disease and related movement disorders. Investigators at Emory University, Massachusetts General Hospital, and The Johns Hopkins University School of Medicine will spend the next five years unraveling the cause or causes of Parkinson's disease and seeking new ways to diagnose and treat it. They will also provide state-of-the-art, multidisciplinary training for young scientists preparing for research careers investigating Parkinson's disease and related neurodegenerative 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.