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OHSU research reveals possible future target for delaying or stopping Alzheimer's
Researchers at Oregon Health & Science University's Neurological Sciences Institute (NSI) have located a possible target for future therapies aimed at delaying or stopping Alzheimer's disease. view more (2006-05-02)
An atomic-level look at an HIV accomplice
Since the discovery in 2007 that a component of human semen called SEVI boosts infectivity of the virus that causes AIDS, researchers have been trying to learn more about SEVI and how it works, in hopes of thwarting its infection-promoting activity. view more (2009-11-20)
Impaired clearance of amyloid-beta causes vascular damage in Alzheimer's disease
New research suggests that accumulation of amyloid-β peptides in cerebral blood vessels, as opposed to the brain itself, may be a more important pathological mediator of Alzheimer's disease. view more (2005-07-21)
Prion disease infectivity causes heart damage in mouse study
Laboratory mice infected with the agent of scrapie—a brain-wasting disease of sheep—show high levels of the scrapie agent in their heart several hundred days after being infected in the brain, indicating that heart infection might be a new aspect of this disease. view more (2006-07-07)
Scientists use Iceland's genealogical database to pinpoint the heritage of a deadly disease
A collaboration of scientists from Iceland and the United States has used Iceland's genealogical database* to trace the ancestors of patients suffering from hereditary cystatin C amyloid angiopathy (HCCAA). Analysis shows that the deadly mutation in the cystatin C gene, L68Q, derives from a common ancestor born roughly 18 generations ago, around... view more... (2008-06-20)
Rethinking Alzheimer's disease and its treatment targets
The standard explanation for what causes Alzheimer's is known as the amyloid hypothesis, which posits that the disease results from of an accumulation of the peptide amyloid beta, the toxic protein fragments that deposit in the brain and become the sticky plaques that have defined Alzheimer's for more than 100 years. view more (2009-09-23)
Calorie restriction may prevent Alzheimer's through promotion of longevity program in the brain
A recent study directed by Mount Sinai School of Medicine suggests that experimental dietary regimens might calm or even reverse symptoms of Alzheimer's Disease (AD). view more (2006-06-15)
Study links Alzheimer's disease to abnormal cell division
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. view more (2006-01-18)
New clues to stroke role in Alzheimer's
Researchers have discovered key details of how stroke or traumatic brain injury can trigger Alzheimer's disease (AD) by enhancing formation of brain-clogging amyloid plaques. view more (2007-06-07)
The good and the bad of a potential Alzheimer's target
Research in fruit flies has shown that enhancing the production of a protein called neprilysin can reduce the formation of plaques and neuron death associated with Alzheimer's, at the expense of reducing the flies' lifespan. view more (2008-06-30)
Alzheimer's: New findings resolve long dispute about how the disease might kill brain cells
For a decade, Alzheimer's disease researchers have been entrenched in debate about one of the mechanisms believed to be responsible for brain cell death and memory loss in the illness. view more (2009-04-16)
Scientists demonstrate means of reducing Alzheimer's-like plaques in fly brain
Neuroscientists at Cold Spring Harbor Laboratory (CSHL) are part of a collaboration that has succeeded in demonstrating that overexpression of an enzyme in the brain can reduce telltale deposits causally linked with Alzheimer's disease. view more (2008-07-16)
Hopkins researchers discover new link to schizophrenia
Neuroscientists at Johns Hopkins have discovered that mice lacking an enzyme that contributes to Alzheimer disease exhibit a number of schizophrenia-like behaviors. view more (2008-05-09)
Enzyme action creates protein linked to Alzheimer's disease
Researchers at UT Southwestern Medical Center have defined a key step in the production of beta-amyloid, a short protein that is thought to be responsible for the development of Alzheimer's disease. view more (2005-08-15)
New findings about brain proteins suggest possible way to fight Alzheimer's
The action of a small protein that is a major villain in Alzheimer's disease can be counterbalanced with another brain protein, researchers at UT Southwestern Medical Center have found in an animal study. view more (2009-10-07)
Penn study finds inhaled anesthetics accelerate the appearance of brain plaque in animals
Researchers at the University of Pennsylvania's School of Medicine have discovered that common inhaled anesthetics increase the number of amyloid plaques in the brains of animals, which might accelerate the onset of neurodegenerative diseases like Alzheimer's. view more (2007-03-12)
Seeing Alzheimer's amyloids
In an important step toward demystifying the role protein clumps play in the development of neurodegenerative disease, researchers have created a stunning three-dimensional picture of an Alzheimer's peptide aggregate using electron microscopy. view more (2008-05-13)
Targeting a key enzyme with gene therapy reversed course of Alzheimer's disease in mouse models
In mice, that had been genetically engineered to develop Alzheimer's disease, scientists were able to reverse the rodents' memory loss by reducing the amount of an enzyme that is crucial for the development of Alzheimer's disease. view more (2005-09-22)
Brain damage found in cognitively normal people with Alzheimer's marker
Researchers at Washington University School of Medicine in St. Louis have linked a potential indicator of Alzheimer's disease to brain damage in humans with no signs of mental impairment. view more (2009-03-11)
Calcium may be the key to understanding Alzheimer's disease
Researchers at the University of Pennsylvania School of Medicine have shown that mutations in two proteins associated with familial Alzheimer's disease disrupt the flow of calcium ions within neurons. The two proteins, called PS1 and PS2 (presenilin 1 and 2), interact with a calcium release channel in an intracellular cell compartment. view more (2008-07-21)
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