P-tau217 appears sooner than p-tau181 in the brain, and it distinguishes AD from controls and other dementias even more cleanly.
By engaging scientists studying every tau-based disorder, a new conference aimed to foster collaborations and research directions.
Tau2020: Meeting for Tauopathies Debuts Genetic Variants Behold the First Human α-Synuclein CryoEM Fibril Structure New at Tau2020: PET Detects First Traces of Tangles in Rhinal Cortex Primary Tauopathies Get New PET Ligands Tau Receptor Identified on ...
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.
The AAT-AD/PD conference hosted a virtual conversation about what the trial’s disappointing cognitive and tantalizing biomarker data might mean. Hidden between thank you’s and pledges to stay committed were substantive points of debate and context.
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.