Representatives of the German Centre for Neurodegenerative Diseases (DZNE), the UK Medical Research Council (MRC) and the Canadian Institutes of Health Research (CIHR) today signed a cooperation agreement that aims to establish and apply harmonised guidelines and technologies for research on neurodegenerative diseases.
Researchers have discovered how mutations in the presenilin 1 gene cause early-onset Alzheimer’s disease (AD). The finding, reported online in the journal Cell, opens the door to developing novel treatments for this form of the mind-robbing disease and for the more common, late-onset form that develops later in life and affects millions of people worldwide.
Patients in the early to moderate stages of Alzheimer’s Disease could have their cognitive impairment slowed or even reversed by switching to a healthier diet.
Older veterans with post-traumatic stress disorder (PTSD) appear more likely to develop dementia over a seven-year period than those without PTSD, according to a report in the June issue of Archives of General Psychiatry, one of the JAMA/Archives journals.
Reducing a protein called beta-amyloid in young mice with a condition resembling Down syndrome improves their ability to learn, researchers at UT Southwestern Medical Center have found.
A surgical treatment that stimulates distressed neural networks through electrodes threaded directly into a person's brain has quietly made a difference in the lives of tens of thousands of people with Parkinson disease, essential tremor, and dystonia over the course of the past decade. What about the mind? Could DBS eventually help other brain diseases such as Alzheimer's? Alzforum reporter Amber Dance investigates in a new four-part series.
Writing the latest pages of an anthropological mystery, scientists propose in this month’s Archives of Neurology that it is highly possible that Auguste Deter, the first identified Alzheimer disease patient, carried the N141I presenilin-2 mutation—the same one as in present-day U.S. families descended from German emigrants who settled near the river Volga in Russia.
Researchers have zeroed in on a protein that may play a role in the progression of Alzheimer’s disease. The team found that increasing levels of the protein prevented the accumulation of an enzyme linked to Alzheimer’s. The strategy may lead to new treatments for the neurodegenerative disease.
APOEε4 gene carriers with alzheimer’s disease have more memory problems; non-carriers troubled with attention, language and executive function.
Although genome-wide analysis identified two genetic variations associated with Alzheimer disease (AD), these variations did not improve the ability to predict the risk of AD, according to a study in the May 12 issue of JAMA.
The world’s scientific community may be one step closer to understanding age-related memory loss, and to developing a drug that might help boost memory, says UAB neurobiologist David Sweatt in an editorial in Science.
Fifty-four percent of liver patients also display neurocognitive impairments such as short term memory loss, a study found. Average score of impaired patients was lower than that of patients with early-stage Alzheimer's disease.
Husbands or wives who care for spouses with dementia are six times more likely to develop the memory-impairing condition than those whose spouses don’t have it, according to results of a 12-year study led by Johns Hopkins, Utah State University, and Duke University. The increased risk that the researchers saw among caregivers was on par with the power of a gene variant known to increase susceptibility to Alzheimer’s disease, they report in the May Journal of the American Geriatrics Society.
Normal Pressure Hydrocephalus (NPH) is a neurological condition which typically affects adults ages 55 and older. An estimated 5.3 million Americans have Alzheimer’s disease (AD). Research analyzes the connection between NPH and AD, studying tau-protein abnormalities of the brain and the efficacy of shunt placement in these patients.
As researchers learn more about how we age, they’re finding that genetics are only half of the story when it comes to developing Alzheimer’s disease.
Using a new mouse model of Alzheimer's disease, researchers at Mount Sinai School of Medicine have found that Alzheimer’s pathology originates in Amyloid-Beta (Abeta) oligomers in the brain, rather than the amyloid plaques previously thought by many researchers to cause the disease.
Forget sun, sand, and surf—it was biomarker pools and a sea change in neurocognitive testing that rejuvenated attendees at the 8th Annual Symposium on Early Alzheimer's, held 12-13 March 2010, in Miami Beach, Florida. Our intrepid reporter Pat McCaffrey brings you a full meeting summary, complete with a slide deck that covers the majority of presentations.
Researchers have identified a gene that appears to increase a person’s risk of developing late-onset Alzheimer’s disease, the most common type of Alzheimer’s disease. The research will be presented as part of the late-breaking science program at the American Academy of Neurology’s 62nd Annual Meeting in Toronto, April 10 – 17, 2010. The gene, abbreviated MTHFD1L, is located on chromosome six.
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