Viral surfaces attract proteins from the extracellular environment of the person they infect. This corona of host proteins makes the virus more or less infective—and promotes amyloid fibrils.
Scientists propose that LATE is a neurodegenerative disease marked by TDP-43 pathology in limbic regions, and memory loss. After death, it can be seen alone or with other pathology.
Scientists know that the retina changes in people with preclinical AD; alas, there is neither consensus nor convergence in the field of retinal imaging. An upcoming initiative aims to determine which measures are most robust.
In response to the peptide, these little cells squeeze capillaries, constricting them. This may contribute to neuronal dysfunction.
Co-sponsors Banner, Novartis, and Amgen announced that they will stop testing CNP520 in two Phase 2/3 studies in people at risk of AD. The drug worsened cognition.
In ADNI, blood marker exposes ongoing neurodegeneration across disease stages.
Long recognized in dendrites, scientists now report that substantial synaptic proteome remodeling happens on the axonal side, too.
A PLCG2 variant that reduces a person’s risk of Alzheimer’s, frontotemporal dementia, and dementia with Lewy bodies also appears to extend longevity.
Serial amyloid and tau scans in cognitively healthy people indicate that the speed at which a person’s tau accumulates best predicts his or her future cognitive decline.
Aβ deposits make distal neurons vulnerable to insults, including from local Aβ, says imaging study. The combination hastens cognitive decline.
New strains have amyloid, neurodegeneration, and neuroinflammation, all against a background of natural genetic variation.
The locus incertus fine-tunes hippocampus neural activity to control memory formation in stressful situations. Could a new understanding of these circuits shed light on memory loss in Alzheimer’s?
An electron microscopy study reveals a jumbled mess of membrane chunks and malfunctioning organelles, bound together by phosphorylated or truncated α-synuclein.
In a research study, one-fifth of healthy people who learned they were at high risk for AD said they might consider physician-assisted death as a future option.
Chemotherapy riles microglia, causing neurons to turn down expression of BDNF, a growth factor necessary for myelination. Restoring BDNF signaling on oligodendrocytes spared myelin and memory loss.