As mice age, a busy receptor-mediated protein transport across the barrier wanes; inhibiting an alkaline phosphatase restores it. Meanwhile, the aging barrier becomes generally leaky to large molecules.
Behold single proteins on the move: Super-resolution microscopy of living cells suggests the infamous protease does not form complexes with other secretases in the plasma membrane—in mouse fibroblasts, that is.
The agency is accepting comments on a draft guidance that updates its recommendations for early AD trials, as well as on its first-ever guidance for ALS drug development.
Technical limitations may have misrepresented the transcriptional state of these cells, obscuring detection of their activation signature in frozen postmortem tissue from Alzheimer’s brain.
In a conditional mouse knockout, lack of neuronal BIN1 slowed excitatory signaling, leading to spatial memory problems. Could this play a role in Alzheimer’s?
In mice lacking the recycling protein GGA3, BACE1 trafficking stalls, local Aβ production increases, and axons swell. Does this explain the neuritic dystrophies seen in early AD?
A newly discovered lipid modification on the amyloid precursor protein may mark it for amyloidogenic processing...
Single-cell RNA sequencing of 16,000 live microglia freshly isolated from human brain reveals nine distinct subtypes. One fades in Alzheimer’s. Why?
Quantifying 95 post-translational modifications of tau extracted from AD and control brains, a proteomics study proposes a “processive” model of phosphorylation, ubiquitination, acetylation that drive aggregation and map to distinct stages of disease.
Among people with early AD, the monoclonal antibody wiped out Aβ plaques and slowed cognitive and functional decline by a third, relative to placebo.
At CTAD, researchers discussed possible paths forward. One option: exploring whether low doses prevent plaque accumulation while avoiding the cognitive side effects.
African Americans are likelier than non-Hispanic Caucasians to carry low-expression TREM2 variants, and less likely to carry a high-expression variant. As a result, they have less soluble TREM2 in their cerebrospinal fluid.
Passive antibody immunization against prion protein prevents the spread of clinical disease to the brain of mice, even though the antibody works primarily by reducing prion replication in peripheral tissues, including the spleen. This is the astonishing news in a report in today’s Nature...
As a number of drug candidates to prevent, slow, or even halt Alzheimer's disease are being developed, a new urgency is driving efforts to develop tests that can diagnose the disease in its earliest stages...
Originally, vaccination with amyloid-β (Aβ) peptides aimed to fight Alzheimer disease by...