Coronavirus Takes Its Toll on Alzheimer’s Clinical Studies
Most observational cohorts are on pause, and many clinical trials have stopped dosing. The long-term effects on the integrity of AD studies are unclear.
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Most observational cohorts are on pause, and many clinical trials have stopped dosing. The long-term effects on the integrity of AD studies are unclear.
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.
At AAT-ADPD, researchers report how they built on prior reports that a person’s blood level of p-tau181 tells if they have Alzheimer’s.
P-tau217 appears sooner than p-tau181 in the brain, and it distinguishes AD from controls and other dementias even more cleanly.
Data shown at AAT-AD/PD explain why the DIAN-TU trial missed its primary endpoint. But gantenerumab strongly reduced plaques, tau, phospho-tau, and slowed NfL. This result prompted an open-label extension, sustaining hope for efficacy.
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.
In a Phase 2 trial, the vaccine reportedly normalized the rise in plasma NfL, and appeared to lower CSF tau and retard brain atrophy.
Scientists report at AAT-AD/PD that they tightened a causal connection between gut microbes, microglial function, and protein deposits. In mice, that is.
Massive meta-analysis finds the longevity gene’s VS haplotype staves off mild cognitive impairment and AD. It reduces amyloid burden.
For people with Parkinson’s, carrying Alzheimer’s genetic risk variants upped their odds of harboring Aβ and tau pathology and getting dementia. In people with DLB, Aβ plaques worsened tau and Lewy pathology, and cognition.
Trialists are shooting new arrows at the disease, including compounds that tweak autophagy, neuroinflammation, and glycolipid recycling.
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.
The first topline Phase 2 results from an antibody targeting Parkinson’s pathology, Roche’s prasinezumab, were a mixed bag. Next steps are unclear.