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DELETIONS IN MITOCHONDRIAL DNA FROM LASER MICRODISSECTED BLOOD VESSELS OF ALZHEIMER BRAINS
Author(s) -
trikamji bhavesh v,
Miller Bradley Bryan
Publication year - 2012
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.26.1_supplement.1035.18
Subject(s) - mitochondrial dna , biology , pathology , alzheimer's disease , mutation , population , disease , genetics , gene , medicine , environmental health
The role of neurovascular dysfunction has long been suggested to be of relevance in the disease pathology of Alzheimer's. However, a mitochondrial genetic cause for vascular dysfunction has yet to be investigated in depth. We examined the mtDNA of individual cerebral endothelial cells obtained by laser micro‐dissection from 9 Alzheimer disease brains in late Braak & Braak topographical stages of pathology. The objective of our study was to detect deletion‐type mutations in the mtDNA by scanning a region of the genome in which deletions have been most commonly detected. We detected 4 separate mtDNA mutations from a total of 18 endothelial cells isolated from 9 Alzheimer brains (2 cells from each). These mutations were characterized by sequence analysis. We suggest that the presence of mtDNA mutations in the small number of endothelial cells from Alzheimer brains indicates that the microvascular cell population may harbor a high aggregate level of such mutations, potentially underlying increasing vascular dysfunction in Alzheimer disease and, possibly, in aging.