Scientists claim to turn differentiated mouse cells into pluripotent ones with a brief dip in an acid bath—no genetic tweaks necessary.
Tau fragments in cerebrospinal fluid might lead to better prognostic and diagnostic tests.
PINK1 mutations cripple mitochondrial energy production, raising new questions about Parkinson’s disease.
An antioxidant thought to boost mitochondrial function came up short in a large multicenter trial for PD treatment.
Exome sequencing identifies a new Alzheimer’s risk gene—phospholipase D3.
A Keystone symposium underscores the role of lysosomal dysfunction and vesicle trafficking in neurodegenerative disease.
Low levels of 10 phospholipids in blood plasma correlated with future cognitive decline in older adults, hinting at diagnostic potential.
A combination of high clusterin and low Aβ42 in cerebrospinal fluid associates with early Alzheimer’s neurodegeneration, hinting at a mechanistic interaction between the proteins.
Eating fewer saturated fats and simple sugars reduces harmful forms of Aβ in the cerebrospinal fluid, scientists report.
Hunting for rare mutations that cause dementia, researchers have spotted, but not yet snagged, some tantalizing candidates.
The overused adage of the fountain of youth rears its head again, as four new studies show how young blood rejuvenates old brain and muscle, pumping up the vasculature, stem cells, and restoring microglia’s appetite for waste products. Researcher are isolating the responsible factors, for example GDF11.
Researchers are increasingly branching out from their old focus on Aβ and tau to understand how these proteins intersect with physiological processes and new genetic regulatory mechanisms in the aging brain.
Do blood components really leak across an inflamed blood-brain barrier early on in the development of Alzheimer’s disease? Some GWAS hits and budding neuro-imaging and fluid markers are helping researchers find out.