One rare variant protects ApoE4 carriers, others put noncarriers at risk.
In Taiwan, interferon treatment for chronic hepatitis C infection appears to have reduced the incidence of Parkinson’s disease.
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?
Serum from young mice boosted synapses and activity in human neurons. Researchers credit the proteins SPARCL1 and THBS4.
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.
Researchers identify a specific SCF ligase that clears fibrillar but not physiologic forms of α-synuclein, suggesting potential for a targeted therapeutic approach.
A compound that only blocks presenilin 1-containing secretases beat back leukemia in mice—without side effects caused by broad-spectrum inhibitors.
Organoids patterned on the dorsal human forebrain consistently contain a set of cells native to the cerebral cortex, and develop along the same trajectory as fetal brains. Could they become the standard for organoid research?
In a mouse model of frontotemporal dementia, a trifecta of tau mutations hobbles newborn neurons in the dentate gyrus.
A PLCG2 variant that reduces a person’s risk of Alzheimer’s, frontotemporal dementia, and dementia with Lewy bodies also appears to extend longevity.
Phase 1b data show that Biogen’s BIIB092 lowers N-terminal tau fragments in cerebrospinal fluid by more than 90 percent.
Scientists link this mysterious form of dementia to higher plasma LDL-cholesterol, and to genetic variants in APOB, which encodes the major component of low-density lipoprotein.
Chemotherapy riles microglia, causing neurons to turn down expression of BDNF, a growth factor necessary for myelination. Restoring BDNF signaling on oligodendrocytes spared myelin and memory loss.
The locus incertus fine-tunes hippocampus neural activity to control memory formation in stressful situations. Could a new understanding of these circuits shed light on memory loss in Alzheimer’s?
Viral surfaces attract proteins from the extracellular environment of the person they infect. This corona of host proteins makes the virus more or less infective—and promotes amyloid fibrils.