New Knock-In Mice Rapidly Accumulate Amyloid Plaques
The APP/PS1 double knock-ins begin to deposit amyloid in the brain by 3 months of age.
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The APP/PS1 double knock-ins begin to deposit amyloid in the brain by 3 months of age.
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.
A new PET tracer. Plasma glial fibrillary acidic protein. Two new, promising surrogates for astrogliosis are filling in the Alzheimer’s biomarker toolbox. Both reflect Aβ amyloid better than they do tau tangles.
Two mouse models presented at AD/PD may hand scientists more translationally relevant tools to explore LOAD pathophysiology and treatment. The tricks: targeted replacement and knocking in multiple GWAS variants.
Incorporation of a cryptic exon scuttles translation of UNC13A, but only in neurons lacking nuclear TDP-43. UNC13A ALS/FTD risk variants exacerbate the aberrant splicing.
In early stage trials, light and sound promoted neuronal communication, calmed immune cells, and slowed brain atrophy, but cognitive benefit remains unclear.