Deficiency in mural vascular cells coincides with blood-brain barrier disruption in Alzheimer's disease.
Level 4 - case-series / case-control
Case-control postmortem human tissue study
PubMed 23126372 · doi:10.1111/bpa.12004
What was done
Postmortem brain tissue from individuals with Alzheimer's disease (AD) and neurologically intact controls was analyzed to evaluate mural vascular cell loss and blood-brain barrier (BBB) integrity. Investigators quantified pericyte number and coverage in the cortex and hippocampus, and measured extravascular deposition of immunoglobulin G (IgG) and fibrin as markers of BBB disruption.
What was found
Compared with neurologically intact controls, AD subjects showed significant reductions in pericyte number and coverage: - Cortex: pericyte number decreased by 59% (P < 0.01) and coverage decreased by 60% (P < 0.01). - Hippocampus: pericyte number decreased by 32% (P < 0.01) and coverage decreased by 33% (P < 0.01). Reductions in pericyte coverage correlated strongly with increased extravascular leakage: - Cortex: correlation with IgG leakage r = -0.96 (P < 0.01); correlation with fibrin deposition r = -0.81 (P < 0.01). - Hippocampus: correlation with IgG leakage r = -0.86 (P < 0.01); correlation with fibrin deposition r = -0.98 (P < 0.01).
Why it matters
The study provides quantitative human pathological evidence linking pericyte loss to cerebrovascular breakdown in AD, supporting mural cell deficiency as a potential contributor to neurovascular impairment.
Limits
The abstract does not report the total sample size (n), participant demographics, postmortem intervals, or disease staging. Because this is a cross-sectional postmortem observational study, it demonstrates correlation rather than a direct causal sequence between pericyte loss and BBB breakdown in living humans.
Cited by
- supports The human hippocampus has fewer pericytes at baseline compared to the cortex.