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.
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.
Researchers use a novel genomic approach to better understand genetic mutations associated with familial Alzheimer's disease.
New technology allows researchers to produce images that predate the formation of amyloid beta in the brain. The findings have prompted researchers to suggest stabilizing the protein, rather than attempting to limit it, in order to reduce Alzheimer's symptoms.
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.
Findings promising as a potential early therapeutic intervention for AD.
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.
Study identifies the main components driving amyloid beta-associated synaptic degeneration.
A new study reports the dementia associated with Down syndrome involves defects in GSAP, which also malfunctions in Alzheimer's disease.
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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.