a(GO:"Lewy body")
We soon found that DF2 strongly stained cortical and brain stem Lewy bodies in brain sections from “diffuse Lewy body disease” (Kuzuhara et al. 1988), as originally described by Kenji Kosaka (1978), who proposed that some elderly subjects dying with dementia had many cortical Lewy bodies PubMed:22908190
The DF2 immunoreactivity of Lewy bodies led us to search for similar DF2-positive inclusions, and we found that Lewy-like bodies in motor neurons in amyotrophic lateral sclerosis (ALS; Murayama et al. 1990a) and Pick bodies in Pick’s disease (Murayama et al. 1990b) were strongly reactive; the latter stained also for tau, whereas the former stained neither for tau nor a-synuclein. PubMed:22908190
The DF2 immunoreactivity of Lewy bodies led us to search for similar DF2-positive inclusions, and we found that Lewy-like bodies in motor neurons in amyotrophic lateral sclerosis (ALS; Murayama et al. 1990a) and Pick bodies in Pick’s disease (Murayama et al. 1990b) were strongly reactive; the latter stained also for tau, whereas the former stained neither for tau nor a-synuclein. PubMed:22908190
We soon found that DF2 strongly stained cortical and brain stem Lewy bodies in brain sections from “diffuse Lewy body disease” (Kuzuhara et al. 1988), as originally described by Kenji Kosaka (1978), who proposed that some elderly subjects dying with dementia had many cortical Lewy bodies PubMed:22908190
In this dementia, Lewy bodies are abundant in cortical neurons, especially in the cingulate gyrus, in addition to their presence in the substantia nigra and locus ceruleus, their prototypical loci in Parkinson’s disease. PubMed:22908190
p62 localizes to a variety of ubiquitin-positive neuropathological inclusions including Lewy bodies in Parkinson’s disease, neurofibrillary tangles in tauopathies, polyglutamine-expanded huntingtin aggregates in Huntington’s disease, and aggregates of mutant SOD1 in familial amyotrophic lateral sclerosis [85–87]. PubMed:18930136
The accumulation of α‐synuclein gives rise to the formation of a nucleus for the accumulation of other proteins, which ultimately leads to the formation of Lewy bodies (within the dopamine secreting cells). PubMed:30663117
We soon found that DF2 strongly stained cortical and brain stem Lewy bodies in brain sections from “diffuse Lewy body disease” (Kuzuhara et al. 1988), as originally described by Kenji Kosaka (1978), who proposed that some elderly subjects dying with dementia had many cortical Lewy bodies PubMed:22908190
The DF2 immunoreactivity of Lewy bodies led us to search for similar DF2-positive inclusions, and we found that Lewy-like bodies in motor neurons in amyotrophic lateral sclerosis (ALS; Murayama et al. 1990a) and Pick bodies in Pick’s disease (Murayama et al. 1990b) were strongly reactive; the latter stained also for tau, whereas the former stained neither for tau nor a-synuclein. PubMed:22908190
We soon found that DF2 strongly stained cortical and brain stem Lewy bodies in brain sections from “diffuse Lewy body disease” (Kuzuhara et al. 1988), as originally described by Kenji Kosaka (1978), who proposed that some elderly subjects dying with dementia had many cortical Lewy bodies PubMed:22908190
In this dementia, Lewy bodies are abundant in cortical neurons, especially in the cingulate gyrus, in addition to their presence in the substantia nigra and locus ceruleus, their prototypical loci in Parkinson’s disease. PubMed:22908190
The DF2 immunoreactivity of Lewy bodies led us to search for similar DF2-positive inclusions, and we found that Lewy-like bodies in motor neurons in amyotrophic lateral sclerosis (ALS; Murayama et al. 1990a) and Pick bodies in Pick’s disease (Murayama et al. 1990b) were strongly reactive; the latter stained also for tau, whereas the former stained neither for tau nor a-synuclein. PubMed:22908190
p62 localizes to a variety of ubiquitin-positive neuropathological inclusions including Lewy bodies in Parkinson’s disease, neurofibrillary tangles in tauopathies, polyglutamine-expanded huntingtin aggregates in Huntington’s disease, and aggregates of mutant SOD1 in familial amyotrophic lateral sclerosis [85–87]. PubMed:18930136
The accumulation of α‐synuclein gives rise to the formation of a nucleus for the accumulation of other proteins, which ultimately leads to the formation of Lewy bodies (within the dopamine secreting cells). PubMed:30663117
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If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.