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Hyperhomocysteinemia (Hcy) predicts small vessel MRI pathology and cognitive impairment with high amyloid‐B‐peptide degrading proteases in the NAME elderly cohort
Author(s) -
Rosenberg Irwin,
Scott Tammy,
Bhadelia Rafeeque,
Qiu Wendy
Publication year - 2013
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.27.1_supplement.346.5
Subject(s) - hyperhomocysteinemia , hyperintensity , dementia , pathology , amyloid (mycology) , medicine , leukoaraiosis , homocysteine , pathogenesis , senile plaques , vascular dementia , alzheimer's disease , cognitive decline , psychology , disease , magnetic resonance imaging , radiology
Although Alois Alzheimer's 1907 description of brain pathology in a pre‐senile dementia patient emphasized vascular pathology with deposition of amyloid‐like substances in brain tissue, current definition of Alzheimer's disease (AD) has often excluded vascular pathogenesis. The relationship between cerebrovascular (CBV) pathologies and the amyloid pathology in AD is also unclear. We have studied 318 multi‐ethnic elderly in the Nutrition Aging and Memory Study (NAME) with nutritional, cognitive, and magnetic resonance imaging assessments and found a relationship of small vessel pathology (infarcts and white matter abnormalities) with high blood homocysteine (Hcy) and cognitive impairments, and also noted an association of small vessel infarcts (SVI) to elevated amyloid‐B‐peptide degrading enzymes. Total CBV pathology, particularly SVI (P=.007) and periventricular white matter hyperintensities (P=.04), was associated with elevated fasting Hcy which was inversely related to measures of executive cognitive function (P=.04). SVI, in turn was related to elevated amyloid‐B‐peptide degrading enzyme activity (P=.02). These observations of small vessel pathology in brain with high Hcy and cognitive impairment and now with B‐amyloid processing emphasize the importance of considering vascular elements of age‐related dementia and even the relations of CBV and B‐amyloid pathogenesis in AD.