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.
Microglial responses to Alzheimer’s risk variants, and to tau pathology, appear to show a sex difference. Microglia in male versus female mice use different biological mechanisms to maintain homeostasis.
At a joint Keystone symposia, researchers reported how microglia, via TREM2, compress plaques and rein in the pathogenic distortion of neurites into swollen stubs. Without TREM2, these damaged neuronal processes served as fertile ground for tau propagation.
Joint Keystone Symposia: Neurodegenerative Diseases: New Insights and Therapeutic Opportunities and Neural Environment in Disease: Glial Responses and Neuroinflammation
TREM2, Microglia Dampen Dangerous Liaisons Between Aβ and Tau Down to Sex? Boy and Girl Microglia Respond Differently Dopaminergic Neurons Conjured from Astrocytes Restore Motion In PD Model, α-Synuclein Spreads from Intestine to Brain Do Microglia Finish ...
In carriers of a PD-causing mutation, PET scans showed serotonin transporter loss before motor symptoms set in.
Through an endocytic process called LANDO, microglia clear β-amyloid and route their used Aβ receptors, including TREM2, back to the plasma membrane. Without it, aggregates pile up outside and form plaques.
Two groups create mice for imaging and manipulation of microglia, leaving related cells untouched. The trick? Piggybacking on Tmem119 expression.
Today, the creators of bioRχiv launch a repository for preliminary medical research, including clinical trial data.
Fully automated immunoassay could offer cost-effective screening for AD.
A meta-analysis of 47 studies suggests CSF NfL is particularly elevated in a select few, suggesting it could help in differential diagnosis.
In response to the peptide, these little cells squeeze capillaries, constricting them. This may contribute to neuronal dysfunction.
New strains have amyloid, neurodegeneration, and neuroinflammation, all against a background of natural genetic variation.
In healthy, older adults specific EEG patterns correlated with plaque and tangle burdens.
Using different techniques, contestants vied for the best way to tell which ADNI participants would develop clinical, cognitive, or imaging signs of Alzheimer’s disease.
Aβ deposits make distal neurons vulnerable to insults, including from local Aβ, says imaging study. The combination hastens cognitive decline.