White-matter hyperintensities, astrocyte damage, hypoperfusion, and amyloid angiopathy draw scrutiny as factors in the complex relationship between cerebrovascular and neurodegenerative processes in dementia.
Ablating Gpr3 reduced amyloid burden and improved memory in various AD mouse models. Researchers propose using Gpr3 inhibitors to treat AD.
Fungal cells cropped up in multiple brain regions of all AD brains examined, but how they got there and what they are doing remains mysterious.
Excess Aβ42 trips up calcium homeostasis and precipitates the loss of spines thought to be important for memory.
When researchers directly convert skin cells into neurons, skipping the stem-cell step, the cells express gene signatures that reflect the age of their donors.
Knocking out interferon-β in mice caused α-synuclein to pile up in neurons, leading to neurodegeneration with features of Parkinson’s disease.
Microglia may transport tau between neurons by taking it up and secreting it in exosomal packages. Blocking exosome synthesis stopped the transfer.
Granules in the nucleus and cytoplasm may owe their genesis and shape to liquefied forms of ALS-linked proteins, such as FUS and hnRNPA1.
Researchers report the first known enzyme that combines disaggregase and protease activity.
A CD33 variant associated with Alzheimer’s boosts levels of wild-type TREM2, hinting that these risk factors could share a common mechanism.
The genetic relics of ancient, dormant retroviruses pepper the human genome. One such virus reanimates in about one-third of ALS cases.
Analysis of the avagacestat trial of 2012 details the side effects that sank the drug, and the outcomes that support CSF biomarkers for prodromal Alzheimer’s disease.
The 1000 Genomes consortium released its final report and sequence data set. It will help scientists studying neurodegenerative diseases better interpret GWAS findings.
Acetylated tau accumulates in Alzheimer’s disease, and associates with pathology and behavioral measures in mouse models.
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.