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Arteriolar ApoE Expression is Increased Alzheimer Disease Cortex.
Author(s) -
Hulette Christine Marie,
Ervin John F,
Steed Emily,
Szymanski Mari,
Burke James,
WelshBohmer Kathleen
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a72-b
Subject(s) - grey matter , apolipoprotein e , white matter , cerebral amyloid angiopathy , pathology , immunohistochemistry , cortex (anatomy) , alzheimer's disease , medicine , anatomy , biology , neuroscience , disease , magnetic resonance imaging , dementia , radiology
Vascular smooth muscle actin (SMA) is reduced in Alzheimer Disease (AD) brain. ( JNEN 2004; 63 :–41). Cerebral amyloid angiopathy (CAA) in AD is increased but does not exactly mirror reduced SMA expression. (Acta Neuopathol Trembath et al In Press ) Because ApoE plays a role in beta amyloid trafficking, we examined arteriolar ApoE expression. ApoE immunohistochemistry and digital image analysis of middle frontal and inferior parietal cortex was used to examine ten ApoE 3,3 and ten ApoE 4,4 AD brains and ten normal control brains matched for age, sex, and duration of disease. ApoE immunoreactivity was lowest in the white matter arterioles. In normal controls, ApoE was greater in the arachnoid vessels than in vessels of the grey and white matter (p<0.0001) and grey matter arterioles exhibited significantly more ApoE staining than those in the white matter (p<0.05). In contrast, in both AD groups, arteriolar apoE was maximal in the grey matter (p<0.0001). Increased ApoE expression in the grey matter arterioles may reflect localization of AD pathology to the cortex. These observations may be important for understanding the increased risk of AD associated with the ApoE‐ε4 allele. Supported by PHS NIA P50 AG05128 and NIA P30 AG028377.