Older adults with amyloid in their brains develop abnormal activity in the entorhinal cortex even while memory and hippocampal function remain unaffected.
If new results hold up, enhanced phosphorylation of a ribosomal protein may explain the toxicity of mutations that cause Parkinson's.
Scientists claim that AV-133, an imaging agent that visualizes dopaminergic neurons, can gauge progression of Parkinson’s disease.
Scientists generate human embryonic stem cell lines from adult donor cells, building on earlier studies that showed this was possible with fetal cells.
European and U.S. agencies approve a third amyloid PET tracer, florbetaben.
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.
A gene already well known to counteract aging appears to improve cognition.
Speakers at Alzheimer’s conference reviewed planned Phase 1 and prevention trials and preclinical studies.
Are New Cognitive Tests Ready For Preclinical Trials? Do Tau Tracers Track Cognitive Decline in Disease? Growth Factor Therapy: Safe in Phase 1, Awaiting Efficacy Data Clinical Trials Conference on Alzheimer’s Disease 2013 ...
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Combining exome sequencing with gene interaction analysis allowed researchers to identify 18 new genes for an inherited movement disorder. This method could lead to genes linked to other neurodegenerative diseases.
Network analysis may explain why people with semantic dementia keep making memories even as their hippocampi degenerate.
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.
A small longitudinal study suggests that atrophy begins in the frontoparietal cortex, not the hippocampus, in early Alzheimer's.