By accounting for harmless variants of known ALS genes, researchers made a downward correction of the genetic risk associated with sporadic cases.
CHCHD10 mutations target mitochondria and TDP-43, while a UBQLN4 allele hits the proteasome.
A review of the latest data hints that blood pressure control, exercise, and cognitive training may preserve memory. But scientists require more convincing before they’ll make concrete recommendations.
The QC enzyme inhibitor reduces production of pyroglutamate Aβ, a particularly toxic, sticky form.
White blood cells from certain Parkinson’s patients react to α-synuclein peptides. Is this autoimmune reaction why the major histocompatibility complex is genetically linked to the disease?
The discovery hints that microglia, rather than neurons, may control much of a person’s genetic susceptibility to Alzheimer’s disease.
In a human cell model, VCP variants trigger a cascade of neuronal disruption and hobble astrocytes’ ability to support motoneurons.
Mutations in certain E. coli genes extend the lives of both normal and Aβ-laden roundworms.
Tomlinson was the first to quantify plaques and tangles in the postmortem brain, launching the modern era of Alzheimer’s research.
New diagnostic guidelines on dementia with Lewy bodies fold in science about sleep and the heart, two aspects that distinguish this disorder from Alzheimer’s and Parkinson’s.
Study of A673T carriers strengthens case for reducing Aβ to prevent AD.
Longitudinal ADNI data revealed that people with elevated Aβ declined toward AD, while those with normal levels maintained their cognitive abilities.
A study suggests DJ-1 may protect against oxidative stress by trimming unwanted sugar modifications from biomolecules.
The protease cleaves three C-terminal fragments of the amyloid precursor protein at different amino acid positions.
The transcriptomes of single immune cells in the mouse brain identify specific disease-associated microglia (DAM), which eat away at Aβ deposits.