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.
At Keystone, researchers described how directly converting astrocytes into neurons within the mouse striatum restored neuron numbers in a model of PD.
Brains of old mice birth fewer neurons when T cells invade the subventricular zone. The immune cells spew inflammatory cytokines that snuff out neurogenesis.
Drug didn’t slow decline in a Phase 2 trial.
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.
TREM2 required for reduction of plaque load in CD33 knockouts.
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.
Going Viral: Alzheimer’s Research at Herpes Conference Herpesvirus: Trigger for Many Brain Pathologies? In light of recent work implicating human herpesviruses in AD, virologists invited Alzheimer’s researchers to join them at the 11th International ...
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 ...
At Quebec conference, researchers considered multiple aspects of herpesvirus biology that may come in to play in AD.