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Dementia Press Releases

Prevention may be essential to reducing racial disparities in stroke

Prevention may be essential to reducing racial disparities in stroke
Thursday, Jun 2, 2016
Blacks between the ages of 45 and 54 die of strokes at a rate that is three times greater than their white counterparts, according to the Reasons for Geographic and Racial Differences in Stroke (REGARDS) study, which looked at stroke incidence and mortality of nearly 30,000 participants over the age of 45 from an ethnically and demographically diverse sample of the U.S. population.

Blueprint Neurotherapeutics logo

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.

Proteasomes and Brain Cell Death

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.

Breaking down BRCA1

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.


Scientists adopt new strategy to find Huntington’s disease therapies
Friday, Aug 7, 2015
Scientists searched the chromosomes of more than 4,000 Huntington’s disease patients and found that DNA repair genes may determine when the neurological symptoms begin. Partially funded by the National Institutes of Health, the results may provide a guide for discovering new treatments for Huntington’s disease and a roadmap for studying other neurological disorders.

Microscope image of ALS and FTD in a mouse

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.

New NIH logo

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.

Light Switching Memories

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.

Boosting brain power

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.

Stressed out motor neuron

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.

Alzheimer's Floodgates

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.

Effect of strain B on mouse cells

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.

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.

Society for Neuroscience 2012 meeting logo

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.

Human iPS cells differentiating into dopaminergic neurons

Patient-derived stem cells could improve drug research for Parkinson's
Wednesday, Jul 4, 2012
Researchers have taken a step toward better drug therapies for Parkinson's disease and Huntington's disease by investigating signs of distress and vulnerability in patient-derived cells. Cells derived from patients with Parkinson's had different responses to drug treatments depending on the type of Parkinson's each patient had. These are the latest advances from the NINDS iPS cell consortia.

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.

A DNA helix

Genetic mutation linked to inherited forms of ALS, dementia
Wednesday, Sep 28, 2011
Researchers have identified the most common genetic cause known to date for two neurological diseases, amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). A mutation in a single gene on chromosome 9 accounts for nearly 50 percent of familial ALS and FTD in Finland, and more than a third of familial ALS in other groups of European ancestry.

A gloved hand holding a petri dish.

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.

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.

Mitochondria and their inner membranes are fragmented in Huntington's disease.

A Mitochondrial Meltdown in Huntington's Disease?
Friday, Jun 17, 2011
A study in Nature Medicine shows that the cellular energy factories known as mitochondria become fragmented in cells affected by Huntington's disease. Normal mitochondria have a dynamic structure, fusing together and splitting apart, but in Huntington's, an enzyme called DRP1 may shift the balance toward splitting. The enzyme could be a target for therapy.

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).

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

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.

NINDS Announces New Spanish-Language Website
Friday, Dec 7, 2007
Free, accurate information on many neurological disorders is now available on a new Spanish-language website from the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health (NIH). The website is available at

Lithium May Offer Relief from Rare but Devastating Neurological Disorders
Thursday, Aug 2, 2007
Lithium carbonate, a compound commonly used to treat depression, might also provide symptomatic relief for a group of inherited movement disorders that includes the fatal disease spinocerebellar ataxia type 1 (SCA1).

Therapeutics for Huntington's and Related Diseases Could Pack a One-Two Punch
Tuesday, Jun 5, 2007
Added to its devastating neurological symptoms, Huntington's disease (HD) carries with it a lesser-known horror. The genetic mutation that causes the disease can grow larger, causing its symptoms – involuntary movements, dementia, and dramatic personality changes – to grow worse across generations and even during a single lifetime. New research sheds light on how the mutation grows and offers hope for locking it down.

Variation in HIV Protein Yields Clues to AIDS-Related Dementia
Thursday, Feb 8, 2007
In a move that could lead to better treatments for neurological complications of AIDS, researchers have identified a protein variant in HIV that is associated with brain infection and dementia in people with 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.

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.

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

Investigators Explore Selective Silencing of Disease Genes
Wednesday, Oct 15, 2003
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.
Fact Sheet

Molecular Fingerprint Predicts HIV-Associated Dementia
Monday, Jun 23, 2003
A new study using a cutting edge research technique called "proteomics protein fingerprinting" shows that HIV patients with dementia have distinct protein patterns in their blood, setting them apart from patients with no symptoms of dementia. The study suggests a possible way to screen HIV patients for the first signs of cognitive impairment.
Fact Sheet

Dystonia Protein Linked to Problem Common in Other Neurological Disorders
Monday, Mar 24, 2003
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.
Fact Sheet

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

NIH Grantees Awarded Nobel Prize in Physiology or Medicine for Brain Research
Monday, Oct 9, 2000
Long-time National Institutes of Health grantees Dr. Eric R. Kandel and Dr. Paul Greengard were awarded the 2000 Nobel Prize in Physiology or Medicine for their discoveries in signal transduction in the nervous system. Together their work has improved treatments for Parkinson's disease, schizophrenia, and depression and holds promise for the improvement of memory in various types of dementia.

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).

Genetics Not Significant to Developing Typical Parkinson's Disease
Tuesday, Jan 26, 1999
Genetic factors do not play a significant role in causing the most common form of Parkinson's disease (PD), according to a study to be published in the January 27, 1999 issue of the Journal of the American Medical Association. This epidemiological study, the largest of its kind to investigate the role of genetic or environmental causes of PD, examined 19,842 white male twins enrolled in a large registry of World War II veteran twins.

Gene for Last Major Form of Batten Disease Discovered
Friday, Sep 19, 1997
Just two years ago, the origins of the fatal childhood neurological disorders called Batten disease were shrouded in mystery, and there were few prospects for effective treatment. Now, for the first time, researchers can describe the genetic underpinnings of all major childhood forms of the disease.

NIH Scientists Identify Gene for Fatal Childhood Disorder, Niemann-Pick Type C: Finding Points to Critical New Steps in Cholesterol Processing
Thursday, Jul 10, 1997
Bethesda, MD -- After decades of work, scientists at the National Institutes of Health have identified a gene alteration associated with the fatal childhood cholesterol disorder Niemann-Pick type C (NPC). Learning how the gene functions may lead to the first effective treatment for the disease and to a fundamental new understanding of how cholesterol is processed in the body.

Scientists Locate Parkinson's Gene
Thursday, Nov 14, 1996
For the first time, scientists have pinpointed the location of a gene they believe is responsible for some cases of Parkinson's disease. Their discovery provides strong evidence that a genetic alteration is capable of causing the disease. The study, published in the November 15 issue of Science,1 sheds light on the mysterious origins of this devastating neurological disease that affects about 500,000 Americans.

Scientists Identify Gene for Spinocerebellar Ataxia 2
Thursday, Oct 31, 1996
Scientists have identified the gene altered in one of the most common hereditary ataxias, spinocerebellar ataxia 2 (SCA2). The discovery allows improved genetic testing and provides new clues about how genetic mutations cause several neurological disorders, including Huntington's disease. The findings are reported by three different groups in the November issue of Nature Genetics.

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.

AIDS Virus Can Infect Neurons
Tuesday, Sep 28, 1993
Using modern genetic techniques that can detect single copies of genes inside intact cells, scientists have uncovered the first conclusive evidence that the AIDS virus (HIV) can infect neurons. And using fetal brain tissue cultures, scientists have identified key substances that turn on the AIDS virus in the brain.

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.

Scientists Link Fatal, Cholesterol-Storage Disorder to Chromosome 18
Monday, Mar 1, 1993
Scientists at the National Institute of Neurological Disorders and Stroke (NINDS) have linked a deadly brain disorder, called Niemann-Pick Type C disease, to a small region of human chromosome 18. These findings, reported in the current issue of Proceedings of the National Academy of Sciences,* may eventually lead to improved diagnosis and treatment for this inherited disorder and yield new insight into the metabolism of cholesterol inside the body's cells.

Study Detects Brain Virus in HIV-Positive Patients
Tuesday, May 5, 1992
Scientists at the National Institute of Neurological Disorders and Stroke (NINDS) have identified a potentially fatal virus in the bloodstream in half of a small group of HIV-positive patients without neurological symptoms, they announced today at the annual meeting of the American Academy of Neurology in San Diego.

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.

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.