A new mass spectrometry analysis provides the most thorough catalog yet of modifications to tau.
Findings suggest a severe blow to the head twists the protein's backbone, which may lead to neurofibrillary tangles.
Clever optical corrections reveal microglia and neurons through the intact mouse cranium.
A C-terminal fragment of APP recruits the protein APPL1 to endosomes, causing the enlarged, overactive vesicles seen early in Alzheimer’s disease.
The foundation recognizes the two researchers for their work on the molecular underpinnings Alzheimer’s disease.
Soluble APPα ramps up early in a mouse model of Fragile X Syndrome, and may promote symptoms of the disease. Blocking the peptide’s production could be a treatment strategy.
In some people, proteins in the cerebrospinal fluid trend toward an Alzheimer’s-like profile as early as age 45.
Mutant SOD1 prevents immature lysosomes from traveling along the axon and from maturing, leaving the cell with no means to clear broken-down mitochondria.
Adult mice walk the straight and narrow without reelin, but are more susceptible to Aβ.
The University of California, San Diego, is suing the University of Southern California and Alzheimer scientists.
New genetic methods make it possible to measure variations in DNA from one brain cell to the next, and to investigate whether these mosaic mutations contribute to disease.
Blocking a family of proteins called cytohesins helped clear toxic SOD1. Scientists speculate the inhibition just might do the same for other proteins linked to neurodegeneration.
A protein that accumulates in the blood of old mice impairs memory and neurogenesis.
A behavioral variant of Alzheimer’s disease is not accompanied by shrinking of the frontal cortex. Rather, these patients have similar patterns of atrophy as those with typical AD.
Methylation of cytosines that do not precede guanine bases in DNA prominently occurs in the brain, but not the rest of the body. This epigenetic mark may play a role in Rett syndrome.