The monoclonal antibody activated TREM2 signaling on mouse microglia. It supported their survival and stimulated their clearance of amyloid plaques.
Not sure where that is? You are not alone. It is a tiny spot deep behind the nose, newly defined by the PET signal of early neurofibrillary tangle deposition. It also prompted a tau-staging scheme.
United Kingdom’s DRI pivots to fight COVID-19. The facility could test 10,000 samples per day.
A survey conducted by the Alzheimer’s Association finds that three-quarters of these physicians had little to no residency training in dementia care.
From caregivers going it alone to understaffed nursing homes on lockdown, people with neurodegenerative disease and their caregivers are feeling enormous strain from the novel coronavirus. They are adapting to the new normal with technology.
Two papers report that phosphorylated tau in the blood distinguishes people with AD from healthy controls and from people with frontotemporal and vascular dementias.
A trial of nearly 20,000 participants found no benefit over five years.
Scientists report at AAT-AD/PD that they tightened a causal connection between gut microbes, microglial function, and protein deposits. In mice, that is.
In a Phase 2 trial, the vaccine reportedly normalized the rise in plasma NfL, and appeared to lower CSF tau and retard brain atrophy.
At Tau2020 conference, scientists implicate LDL receptor-related protein 1 in cell-to-cell transmission.
In a mouse model of amyloidosis, human wild-type TREM2 kept Aβ deposition at bay early on, but this defense became overwhelmed as plaques grew. The R47H AD risk variant never offered protection early on, and made things worse later.
New Assay, New Cohorts—Plasma p-Tau181 Looks Even Better 217—The Best Phospho-Tau Marker for Alzheimer’s? In DIAN-TU, Gantenerumab Brings Down Tau. By a Lot. Open Extension Planned Confused About the DIAN-TU Trial Data? Experts Discuss Active Tau Vaccine: ...
Researchers at the online AAT-AD/PD meeting touted therapies that target neuroinflammation, synapses, epigenetic regulation, or the cortisol stress response.
For several neurodegenerative diseases, scientists identified which cell types exert a person’s inherited risk. In Alzheimer’s, it’s microglia; in Parkinson’s, it’s dopaminergic and enteric neurons—and oligodendrocytes.
Trialists are shooting new arrows at the disease, including compounds that tweak autophagy, neuroinflammation, and glycolipid recycling.