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F2‐03‐02: Neuroinflammation as an Early Event and Prime Mover in Alzheimer's Pathobiology
Author(s) -
Town Terrence
Publication year - 2011
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2011.05.831
Subject(s) - neuroinflammation , microglia , inflammation , gliosis , amyloid (mycology) , neuroscience , amyloid precursor protein , amyloidosis , biology , protein tyrosine phosphatase , senile plaques , immunology , pathology , alzheimer's disease , medicine , microbiology and biotechnology , disease , signal transduction
such that individuals with greater coronary risk showed more evidence of brain Abeta deposition (R2 1⁄4 0.16, p 1⁄4 0.008). This relationship was not explained by ApoE genotype, age, or sex. However, in a related study of 47 cognitively normal participants, we did not find evidence for a relationship between CVD and Abeta, as CVD+ vs CVDsubjects did not differ on measures of PIB uptakewhen examined as either a categorical or continuous variable. CVD, however, was associated with significantly poorer performance on a number of cognitive tests while PIB was not. Conclusions: These results demonstrate associations between vascular risk and Abeta, but not between cerebrovascular disease and Abeta. Cerebrovascular disease appears to have greater effects on cognition than Abeta in cognitively normal individuals. These associations could be explained by differences in the relationships in cognitively normal as opposed to cognitively impaired individuals, or it could reflect the fact that vascular risk operates through mechanisms not captured by traditional measures of cerebrovascular disease.