Death receptor role in Alzheimer's disease looks less likely than was originally thought following a high-profile paper in 2009.
A gene already well known to counteract aging appears to improve cognition.
Deep-brain stimulation of the nucleus basalis of Meynert appeared safe and tolerable for Alzheimer’s patients.
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.
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.
European and U.S. agencies approve a third amyloid PET tracer, florbetaben.
A small longitudinal study suggests that atrophy begins in the frontoparietal cortex, not the hippocampus, in early Alzheimer's.
By finding differences in gene expression between monocytes and T cells, scientists reveal that the innate immune system has strong ties to neurodegenerative disease.
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.
Baby Boomers, keep your blood pressure down. Research is beginning to explain how even mild hypertension, a mid-life risk factor for late-life dementia, might be damaging the neurovascular unit.
Marek-Marsel Mesulam received the prestigious award for his research on primary progressive aphasia, a language disorder that can affect people with Alzheimer’s or frontotemporal dementia.
Scientists generate human embryonic stem cell lines from adult donor cells, building on earlier studies that showed this was possible with fetal cells.
Scientists claim that AV-133, an imaging agent that visualizes dopaminergic neurons, can gauge progression of Parkinson’s disease.
Tirasemtiv, a drug thought to make muscles more sensitive to signals from motor neurons, failed to improve muscle function in people with amyotrophic lateral sclerosis.