Proteomics Dates Endosomal, Synaptic Changes to Preclinical AD
In postmortem brain, proteins involved in all manner of vesicular functions waxed or waned with increasing phases of disease, starting years prior to symptoms.
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In postmortem brain, proteins involved in all manner of vesicular functions waxed or waned with increasing phases of disease, starting years prior to symptoms.
Instead of chewing up and disposing of the amyloid they ingest, microglia appear to compact it, then spit it back out as dense-core plaque.
Sending low-intensity, gamma frequency electric current through the brain boosted short-term memory, perhaps by increasing cholinergic transmission.
Herpes infection upped risk in ApoE4 carriers, damaged brain tissue, and correlated with neurodegeneration markers in the CSF.
Disruption of the membraneless organelles may explain toxicity of tau aggregates.
In cell culture, neurons with the strongest expression of cell-cycle proteins survived best in the presence of Aβ oligomers.
In early stage trials, light and sound promoted neuronal communication, calmed immune cells, and slowed brain atrophy, but cognitive benefit remains unclear.
After news on “new data” they won’t see, three committee members argue against approval.
In therapy-like paradigm, suppressing ApoE4 in astrocytes toned down tauopathy. This assuaged microglia, neurodegeneration, and revived nest-building.
New research implicates IL-6 signaling and even Aβ42 itself as BACE targets, complicating efforts to resurrect BACE inhibitors at a low dose.
Data from Phase 3 trials of elenbecestat show no harm to cognition, leaving open a chance that the drugs could be used safely in the future.
The first whole-genome manipulation of protein expression in neurons by CRISPR reveals a deadly chain of events. Bad processing by lysosomes leads to build-up of lipids and iron. Oxidative stress revs up. Neurons die by ferroptosis.
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.
By shifting to home nursing and telemedicine, clinical researchers kept inching ahead during lockdowns.
At AD/PD 2021, clinicians discussed neurological symptoms and brain tissue damage in older people who died from COVID-19.