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Injecting α-synuclein fibrils into mouse gut sparked the proteopathic spread of misfolded α-synuclein into the brain, where the aggregates killed dopaminergic neurons and caused motor problems.
Co-sponsors Banner, Novartis, and Amgen announced that they will stop testing CNP520 in two Phase 2/3 studies in people at risk of AD. The drug worsened cognition.
At Quebec conference, human herpesvirus experts devoted a day to consider whether their favorite villain might play a hand in Alzheimer’s pathogenesis.
TREM2 required for reduction of plaque load in CD33 knockouts.
Drug didn’t slow decline in a Phase 2 trial.
Brains of old mice birth fewer neurons when T cells invade the subventricular zone. The immune cells spew inflammatory cytokines that snuff out neurogenesis.
USC has agreed to compensate UCSD $50 million for poaching Aisen, his staff, and ADCS.
At Keystone, researchers described how directly converting astrocytes into neurons within the mouse striatum restored neuron numbers in a model of PD.
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.
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.
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