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.
Analysis of a chimeric mouse shows that the cells express the same genes they do in the human brain, survey their environment, and respond to injuries and amyloid.
Much of the neuron loss in rTg4510 mice comes from accidental disruptions in mouse genes rather than expression of mutant tau. Pathology spreads quickly in human tau knock-ins.
Thousands of stretches of the genome go undetected by standard short-read sequencing techniques. Unmasking these “dark regions” revealed a potential AD risk variant in the CR1 gene.
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.
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?
Researchers identify a specific SCF ligase that clears fibrillar but not physiologic forms of α-synuclein, suggesting potential for a targeted therapeutic approach.
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?
In healthy, older adults specific EEG patterns correlated with plaque and tangle burdens.
Serum from young mice boosted synapses and activity in human neurons. Researchers credit the proteins SPARCL1 and THBS4.
A meta-analysis of 47 studies suggests CSF NfL is particularly elevated in a select few, suggesting it could help in differential diagnosis.
Fully automated immunoassay could offer cost-effective screening for AD.
In a large observational study, men given androgen-deprivation therapy to combat prostate cancer had a higher chance of being diagnosed with Alzheimer’s or dementia within eight years.
In carriers of a PD-causing mutation, PET scans showed serotonin transporter loss before motor symptoms set in.
USC has agreed to compensate UCSD $50 million for poaching Aisen, his staff, and ADCS.