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.
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 ...
At Quebec conference, researchers considered multiple aspects of herpesvirus biology that may come in to play in AD.
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.
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 At a joint Keystone ...