Familial Alzheimer’s Gene Alters Children’s Brains
In children as young as 9 who carry a presenilin 1 mutation, researchers detect subtle functional and structural brain changes.
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In children as young as 9 who carry a presenilin 1 mutation, researchers detect subtle functional and structural brain changes.
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.
Adult mice walk the straight and narrow without reelin, but are more susceptible to Aβ.
The intracellular domain of the amyloid precursor protein may alter gene expression to reduce production of Aβ.
Decades after getting injections of human growth hormone from brain donors, some people developed amyloid pathology that researchers attribute to transmission of Aβ seeds hidden in the injections.
Micro-electron diffraction reveals atomic resolution of β-sheet structure in an α-synuclein crystal, while a close-up of Aβ fibrils surprises with turns shaped like a tilde.
Mouse studies show the peptide damages the borders between the circulation and central nervous system, but also find that a weakened wall helps clear Aβ from the brain.
Drosophila were just fine, thank you very much, despite carrying the ALS- and FTD-linked repeats in the same intronic context as they occur in people.
Acetylated tau accumulates in Alzheimer’s disease, and associates with pathology and behavioral measures in mouse models.
Altered responses to visual stimuli could signify the extent of TDP-43 pathology in the brain, researchers predict.
Researchers detect liaisons between amyloid precursor protein and β-secretase in Golgi-derived vesicles and recycling endosomes, providing clues to where Aβ could form.
Lawmakers have earmarked an additional $350 million for Alzheimer’s research, the largest increase in history.
Nicastrin selects substrates for γ–secretase by turning away proteins with large ectodomains.
Genetic deletion of white blood cells in an Alzheimer’s mouse model quadrupled plaque load, but restoring peripheral antibodies halved this increase.
Exercising the brain and body in middle age may not limit progression of Alzheimer’s pathology.
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