Leaders protest recent decision to deny Medicare beneficiaries coverage of amyloid scans.
The proportion of seniors with dementia in England appears to be on the decline, new research suggests.
Researchers at AAIC 2013 report that an individual’s subjective sense of worsening memory could be an important predictor of cognitive impairment and dementia.
The route to early dementia starts in adolescence, with low cognitive function and alcohol intoxication as major predictors.
By tracking Alzheimer’s research funding internationally, a new database could help sponsors coordinate research efforts.
Cloistered Retreat Takes the Pulse of BACE Research BACE—Substrates, Functions, Developmental Phenotypes Blocking BACE—Do Adult Mouse Phenotypes Predict Side Effects? Meeting Explores Complex Biology of BACE Regulation BACE Proteases in Health and Disease ...
It’s Not All About You, Neurons. Glia, Blood, Arteries Shine at Symposium Fluid Markers and Imaging Back Idea of Breached Blood-Brain Barrier In Revival of Parabiosis, Young Blood Rejuvenates Aging Microglia, Cognition Glymphatic Flow, Sleep, microRNA Are ...
Nucleotide repeat expansions in the C9ORF72 gene occur in amyotrophic lateral sclerosis and frontotemporal dementia. Now researchers find the same repeats in patients with two other neurological disorders.
Thought to be no place for translation, RNA granules that form in “FUSopathies” turn out to host protein synthesis, after all.
First-generation γ-secretase modulators are less potent in human neurons than in some other cell types, possibly explaining why these drugs failed in clinical trials.
Exome sequencing identifies a new Alzheimer’s risk gene—phospholipase D3.
It’s not just for tugging APP around the neuron: The SORLA receptor may also bind Aβ and hasten its demise.
In a cell culture system, astrocytes from people with ALS kill motor neurons. The model could yield more discoveries about the fundamental biology of this disease.
Researchers have identified the striatum as a site of neurogenesis in the adult brain, but not in people with Huntington’s disease.
In Fragile X syndrome, mRNA from the mutant FMR1 gene binds to its own DNA to suppress protein expression. Could the same thing happen in other repeat expansion diseases?