Parsing Local and Distal Aβ Shows Links to Metabolism, Cognition
Aβ deposits make distal neurons vulnerable to insults, including from local Aβ, says imaging study. The combination hastens cognitive decline.
NEWS
Sliced by ApoE Genotype, Whole Exome Data Yield New AD Variants
One rare variant protects ApoE4 carriers, others put noncarriers at risk.
Study Strengthens Link between Hepatitis C Virus, Parkinson’s
In Taiwan, interferon treatment for chronic hepatitis C infection appears to have reduced the incidence of Parkinson’s disease.
Dead Microglia Pave the Way for Myelin Regeneration
In mice, inflammatory microglia must die, and new ones take over for efficient remyelination. Could problems with this changing of the guard contribute to neurological diseases?
Two Proteins in Young Blood Give Synapses a SPARC
Serum from young mice boosted synapses and activity in human neurons. Researchers credit the proteins SPARCL1 and THBS4.
Serial PET Nails It: Preclinical AD Means Amyloid, Tau, then Cognitive Decline
Serial amyloid and tau scans in cognitively healthy people indicate that the speed at which a person’s tau accumulates best predicts his or her future cognitive decline.
Ubiquitin Ligase SCarFs Up Internalized α-Synuclein, Prevents Seeding
Researchers identify a specific SCF ligase that clears fibrillar but not physiologic forms of α-synuclein, suggesting potential for a targeted therapeutic approach.
γ-Secretase Revisited—Could Selective Inhibitors Treat AD, Cancer Safely?
A compound that only blocks presenilin 1-containing secretases beat back leukemia in mice—without side effects caused by broad-spectrum inhibitors.
Virtual Exhibit Hall
Alzforum encourages users to visit the Virtual Exhibit Hall, where companies showcase their newest initiatives, products, and services. We welcome Dash Genomics, Inc. and Abcam, which join our other exhibitors — Biogen, BioLegend, BrainXell, NanoString Technologies, and the Jackson Laboratory.
SPOTLIGHT
Dead Microglia Pave the Way for Myelin Regeneration
In mice, myelin repair seems efficient only when pro-inflammatory microglia perish and pro-regenerative ones take their place. The old cells die by necroptosis, a type of programmed cell death. Microglial necroptosis and regeneration occur at sites of myelin repair in multiple sclerosis models. It remains to be see whether a similar cellular switcheroo happens in people or in other diseases that cause demyelination, including Alzheimer’s.
Acting Locally and Globally, Aβ Sets Stage for Neurodegeneration
Though amyloid plaques are a hallmark of Alzheimer’s disease, their distribution has never correlated well with cognitive decline. Now, scientists think they know why. According to new research, plaques weaken distant, connected neurons, making them vulnerable to stress. Nearby plaques then disrupt those vulnerable neurons, causing learning and memory problems. The study suggests that global and local A conspire to bring about dementia.
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