作者: Sony Soman
DOI:
关键词: Alzheimer's disease 、 DNA oxidation 、 Polymerase chain reaction 、 Mitochondrial DNA 、 Dementia with Lewy bodies 、 Biology 、 Cancer research 、 DNA repair 、 Oxidative stress 、 Frontotemporal dementia
摘要: OF DISSERTATION OXIDATIVE DAMAGE TO DNA IN ALZHEIMERS DISEASE Previous studies from our laboratory and others show a significant increase in levels of both nuclear mitochondrial RNA oxidation vulnerable brain regions the progression Alzheimer’s disease (AD). Although total is increased AD it remains unclear whether oxidative damage widespread throughout genome or concentrated to specific genes. To test hypothesis that genes are more highly oxidized AD, we propose quantify percent coding for proteins shown be altered using quantitative/real-time polymerase chain reaction (qPCR/ RT-PCR). further diminished repair capacity contributes will use custom PCR arrays qPCR, Western blot analysis activity assays changes enzymes involved base excision (BER). In order carry out these tissue specimens superior middle temporal gyri (SMTG) inferior parietal lobe (IP), as well as, non-vulnerable region, cerebellum (CER) analyzed normal control (NC) subjects including those with preclinical (PCAD), mild cognitive impairment (MCI), late stage (LAD). We also analyze diseased (DC; Frontotemporal dementia (FTD) Lewy bodies (DLB)) determine if observe specific.