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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)

Post-mortem pathological and biochemical studies are reported on six patients with progressive dementia. The characteristic pathological finding was neurofilament-containing cytoplasmic inclusions in cortical and subcortical neurons. The clinical and pathological findings were consistent with so-called diffuse Lewy body disease. The patients had variable changes of the Alzheimer type, with five of six patients displaying "plaques only" Alzheimer's changes. Biochemical studies showed profound decreases in neocortical choline acetyltransferase (ChAT) activities that correlated with marked neuronal loss in the basal nucleus of Meynert. ChAT activities were normal in the hippocampus in three patients who also had no significant Alzheimer type hippocampal changes. All patients had decreased cortical somatostatin-like immunoreactivity. Our observations suggest that dementia in diffuse Lewy body disease bears biochemical similarities to Alzheimer's disease, in that biochemical markers for both intrinsic cortical neurons and ascending cholinergic neurons are affected.
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PMID:Diffuse Lewy body disease. Neuropathological and biochemical studies of six patients. 343 18

We have studied the brains of 10 patients with clinically and pathologically defined Huntington's disease and graded the degree of striatal pathology according to the Vonsattel grading system. Sections from nine cerebral cortical areas (Brodmann areas 8, 10, 24, 33, 28, 38, 7, 39, 18), the cerebellum, hypothalamus, medulla and caudate nucleus were stained with antibodies to ubiquitin and ubiquitin C-terminal hydrolase (PGP 9.5). Dystrophic neurites, immunoreactive with ubiquitin and PGP 9.5 were detected in all cortical areas, in layers 3, 5 and 6, of all brains studied. No dystrophic neurites were found in subcortical areas or cerebellum. Sections from cortical areas 8 and 24 from the two brains with the most and least ubiquitin-immunoreactive neurites were stained with antibodies to beta-amyloid precursor protein, tau, glial fibrillary acidic protein, neurofilament protein, alpha B crystallin, GABA, cholecystokinin and somatostatin. The dystrophic neurites were found to also react with beta-amyloid precursor protein. Electron microscopy showed the abnormal neurites to contain granulofilamentous material. Granular deposits with a diameter of 40-100 nm were interspersed between randomly orientated 'fuzzy' or coated, straight or slightly curved filaments measuring 10-15 nm in diameter. These structures have not been seen in control brain and differ from age-related neuritic degeneration and neurites associated with amyloid. Immunohistochemically these structures most resemble CA 2/3 neurites seen in Lewy body disease, and, ultrastructurally, the intraneuronal filamentous inclusions in motor neuron disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The cortical neuritic pathology of Huntington's disease. 777 Jan 16