APP, a protein commonly associated with Alzheimer's disease, plays a vital role in learning, memory, and social behavior in the developing brain, a new mouse study finds.
Researchers identified gene recombination in neurons that produces new gene variants in the brains of those with Alzheimer's disease. The findings, researchers say, may point to a potential near term treatment for the neurodegenerative disease.
Scientists found diverse genomic changes in single neurons from the brains of Alzheimer’s patients, pointing to an unexpected factor that may underpin the most common form of the disease.
Researchers have implicated a new culprit in the development of Alzheimer's disease. The findings could influence new strategies for treatment.
Researchers use a novel genomic approach to better understand genetic mutations associated with familial Alzheimer's disease.
A new drug has proven effective at restoring memories and neural connections in mouse models of Alzheimer's disease. The new drug was originally developed as a treatment for Schizophrenia. While the drug does not destroy amyloid plaques associated with Alzheimer's, it does allow the plaques to co-exist with neurons.
A new study of the genetic data from over 94,000 people with Alzheimer's has identified five new risk genes, as well as confirmed 20 other known genes in the disease.
Blocking the breakdown of a specific fat molecule in the the brains of mice lead to reduced learning ability and memory retention. Additionally, researchers noted an increase of Alzheimer's related proteins. Findings may help explain how dementia may develop in humans, researchers say.
Researchers report of creating two new mouse models of Alzheimer's disease. They believe the models could potentially revolutionize research into the neurodegenerative disease.
Using a technique called parabiosis on pairs of mice, researchers discover what they call 'cancer like mobility' of amyloid beta, reporting it can travel to the brain from other parts of the body.
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Researchers provide evidence that certain species of human herpesvirus contribute to the development of Alzheimer's disease. The study reports high levels of human herpesvirus 6A and 7 were found in brain samples showing signs of Alzheimer's neuropathology. The findings offer hints of the viral mechanisms that could trigger or exacerbate AD.
Researchers injected a modified segment of the amyloid precursor protein into mouse models of Alzheimer's disease. The treatment appeared to reverse a number of the cognitive and memory problems associated with the neurodegenerative disease.
