Cerebral Small Vessel Disease in Sporadic and Familial Alzheimer Disease.
Level 5 - mechanism / opinion, no new human data
Narrative review synthesizing neuropathological and neuroimaging literature without systematic methodology.
PubMed 34331941 · doi:10.1016/j.ajpath.2021.07.004
What was done
This review synthesized neuroimaging and post-mortem evidence evaluating the prevalence, distribution, and clinical impact of cerebral small vessel disease (SVD) and cerebral amyloid angiopathy in both sporadic and familial Alzheimer disease (AD).
What was found
The abstract reports no numerical data or effect estimates. It reports that white matter hyperintensities (especially frontal periventricular and posterior distributions associated with cerebral amyloid angiopathy in familial AD) frequently occur across the AD spectrum. Additionally, post-mortem studies show that arteriolosclerosis, small cortical and subcortical infarcts, microinfarcts, microbleeds, perivascular spaces, and white matter attenuation are common in both sporadic AD and mutation-confirmed familial AD, shifting the threshold for clinical cognitive impairment.
Why it matters
Pathological and imaging features of vascular disease regularly accompany classic AD biomarkers, supporting the inclusion of SVD markers in the biological definition of AD and highlighting vascular risk management as a therapeutic target.
Limits
The abstract describes a narrative review without detailing search criteria, study selection methods, or participant numbers. No primary quantitative data, effect sizes, or definitive chronological sequences between SVD and classical AD biomarkers are provided.
Cited by
- supports A substantial proportion of patients diagnosed with small vessel disease exhibit cerebral amyloid angiopathy or amyloid plaques upon postmortem brain tissue analysis.