Mechanistic description
Pericyte loss in Alzheimer’s disease leads to proteolytic shedding of PDGFRβ into circulation, providing a blood-accessible marker of pericyte injury. Circulating PDGFRβ correlates with BBB permeability and cognitive decline. Critical weakness: PDGFRβ is not pericyte-specific (expressed on vascular smooth muscle cells, fibroblasts, hepatic stellate cells), making source attribution essential before clinical deployment.
Evidence for (8)
Pericyte loss precedes neurodegeneration in AD models
Circulating PDGFRβ reflects pericyte coverage in human cohorts
PDGFRβ polymorphisms associated with AD risk
Neurovascular pathways to neurodegeneration in Alzheimer's disease and other disorders.
The blood-brain barrier in systemic inflammation.
Role of Blood-Brain Barrier in Alzheimer's Disease.
The blood-brain barrier in Alzheimer's disease.
Blood-Brain Barrier Breakdown in Alzheimer's Disease: Mechanisms and Targeted Strategies.
Evidence against (3)
PDGFRβ+ perivascular fibroblasts distinct from pericytes complicate pericyte-specific attribution
Pericyte coverage changes in aging are highly variable and don't always correlate with cognitive outcomes
AD risk association was modest (OR ~1.3) and not replicated in independent cohorts
Bayesian persona consensus
scidex.consensus.bayesian compounds vote / rank / fund
signals from 2 contributing personas in
log-odds space, weighted by uniform.
Prior 50%.