Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0752347 (Dementia with Lewy bodies)
 1,653 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Oxidative stress is well accepted as an important pathogenic factor in Parkinson disease, based largely on indirect evidence. Recently, we have developed antibodies that recognize specific advanced glycation end-products (anti-pentosidine and anti-pyrraline), protein modifications that are potentiated by oxidative stress in a process termed glycoxidation. We applied these antibodies immunocytochemically to affected regions in Parkinson disease and diffuse Lewy body disease brains. Additionally, we used antibodies to heme oxygenase-1, a putative marker of oxidative stress response. Immunoreactivity to pentosidine, pyrraline, and heme oxygenase-1 was seen in the substantia nigra of Parkinson disease and the neocortex of diffuse Lewy body disease. Heme oxygenase-1 was further demonstrated by immunoelectron microscopy in intimate association with filaments of cortical Lewy bodies. Immunolocalization of advanced glycation end-products and a marker of oxidative stress response induction provides evidence that glycoxidation and oxidative stress may be an important pathogenic factor in diseases characterized by Lewy body formation, and furthers the evidence that cytoskeletal proteins and their inclusions are susceptible to oxidative stress.
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PMID:Glycoxidation and oxidative stress in Parkinson disease and diffuse Lewy body disease. 893 Mar 66

Heme-a, is the heme prosthetic group of cytochrome c oxidase (COX), the terminal complex of the mitochondrial electron transport chain. We measured heme-a levels in postmortem brain tissue from nine patients diagnosed with dementia: Alzheimer's disease (AD) was the primary diagnosis in five, AD/diffuse Lewy body disease (DLBD) was diagnosed in two, DLBD was diagnosed in one, and DLBD (severe)/AD (mild) was diagnosed in one. Eight non-demented patients who died from non-neurological causes served as controls. When the primary diagnosis was AD (AD and AD/DLBD), levels of cerebral heme-a were increased almost two-fold on a protein basis compared to controls (p<0.001). Using perfused and non-perfused rats we showed that measured levels of cerebral heme-a were unaffected by the presence of blood in brain tissue. In mice we showed that levels of cerebral heme-a were unaffected by 24h of storage at 4 degrees C prior to freezing. These animal studies suggest that increased levels of cerebral heme-a in AD were not due to blood in postmortem brain or variation in postmortem interval.
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PMID:Heme-a, the heme prosthetic group of cytochrome c oxidase, is increased in Alzheimer's disease. 1953 9