The Food and Drug Administration has said it will accept cognition alone as the basis for approval in preclinical AD. Now what? Industry is confronting the challenge to show robust and meaningful change.
A broadening drug development pipeline now contains Phase 1 or 2 drugs on targets unrelated to Aβ or tau.
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.
Biogen showed results from clinical trials of anti-Aβ and anti-α-synuclein antibodies at the American Academy of Neurology annual meeting.
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.
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.
Data on ASOs, presented recently at the annual meeting of the American Academy of Neurology, depict RNA-based therapies as broadly on the rise in neurodegenerative diseases.
In hunting for mutations that cause ALS, researchers discovered that VCP mutations, long thought to spare the spine, are instead a cause of inherited ALS...
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.
Brain imaging and cognitive tests may be the gold standards for tracking AD progression, but clinical trials using these procedures are expensive, risky, and time-consuming...
Risk alleles of SORL1 dampen its expression in response to growth factors, leading to higher Aβ production.