Carriers of a rare hypomorphic gene variant develop a frontotemporal dementia that features Alzheimer’s-like neurofibrillary tangles.
The first steps of endocytosis faltered in astrocytes expressing ApoE4, but pumping in PICALM reversed the problem. A new study places two Alzheimer’s risk factors into the same cellular mechanism.
The panel considered the evidence for efficacy to be weak, and was troubled by too-close collaboration between the sponsor and the FDA.
Learning tests may prove more informative in clinical trials of early AD. A new one claims it can spot a difference in six days.
Single-nucleus transcriptomics of postmortem AD brain and mouse models of amyloidosis hammers home the species-specific responses of microglia to Aβ pathology.
Biogen researchers claim the antibody worked in people who got enough of it. To other researchers, the signal validates the amyloid hypothesis and injects fresh energy into the field. But is this interrupted dataset enough to approve?
Hippocampal imaging and fluid markers of BBB damage found in ApoE4 carriers.
With experiments and careers on hold, scientists working from home are turning to virtual lab meetings and journal clubs to keep up morale.
When these tiny mural cells carried APOE4, they secreted more ApoE, causing Aβ to deposit in capillary walls. Blocking ApoE production prevented angiopathy.
Live imaging of mouse brain reveals that microglia quickly engulf cell bodies while astrocytes dispose of the neuron’s more distal reaches. The cleanup crew tires with age.
According to a structural analysis, fluorescently tagged tau fragments cannot form paired helical filaments. This suggests the assay does not measure prion-like propagation.
In mice with defective PS1 phosphorylation, microglial autophagy falters, exacerbating Aβ burden.
The first high-resolution look at LRRK2 implies that pathogenic mutations increase binding to microtubules by biasing the kinase domain toward a closed, active conformation.
A C9ORF72 polydipeptide repeat induces aggregation by direct interaction with TDP-43, while progranulin mutations that trigger microglial toxicity cause TDP-43 to accumulate via complement.
While one anti-Aβ antibody thwarts initial seeding of fibrils, and others keep fibrils from lengthening, aducanumab prevents oligomers forming on their surface. In vitro, that is.