Journal ArticleDOI
Lewy bodies contain beta-amyloid precursor proteins of Alzheimer's disease
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TLDR
To assess the contribution of Alzheimer's disease amyloid proteins to cortical and substantia nigra Lewy bodies (LBs), regions of postmortem brain rich in intraneuronal LBs were examined immunohistochemically and showed that only BAPP epitopes outside the BAP were present in substantia Nigral and cortical LBs.About:
This article is published in Brain Research.The article was published on 1992-07-10. It has received 46 citations till now. The article focuses on the topics: Lewy body & Amyloid precursor protein.read more
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Oxidative stress: Free radical production in neural degeneration
TL;DR: The oxidative stress theory of neurodegeneration, on excitotoxin-induced cell damage and on impairment of mitochondrial function are focused on as three major noxae being the most likely causes of cell death either independently or in connection with each other.
Journal ArticleDOI
The Lewy body in Parkinson's disease: molecules implicated in the formation and degradation of alpha-synuclein aggregates.
TL;DR: The histological hallmark of Parkinson's disease (PD) is the presence of fibrillar aggregates called Lewy bodies (LBs) as discussed by the authors, which is considered to be a marker for neuronal degeneration, because neuronal loss is found in the predilection sites for LBs.
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Abnormal accumulation of NACP/alpha-synuclein in neurodegenerative disorders
TL;DR: The view that NACP specifically accumulates in diseases related to Lewy bodies such as Lewy body variant of Alzheimer's disease, diffuseLewy body disease, and Parkinson's disease is supported and suggests a role for this synaptic protein in the pathogenesis of neurodegeneration.
Journal ArticleDOI
The Lewy Body in Parkinson’s Disease and Related Neurodegenerative Disorders
TL;DR: The histopathological hallmark of Parkinson’s disease is the presence of fibrillar aggregates referred to as Lewy bodies (LBs), in which α-synuclein is a major constituent, and recent studies have indicated that nonfibrillars α- synuclein are cytotoxic and that fibrillsar aggregate ( LBs and pale bodies) may represent a cytoprotective mechanism in PD.
Journal ArticleDOI
Microglia enhance β‐amyloid peptide‐induced toxicity in cortical and mesencephalic neurons by producing reactive oxygen species
TL;DR: This study demonstrates that one of the mechanisms by which microglia can enhance the neurotoxicity of Aβ is via the production of reactive oxygen species.
References
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Journal ArticleDOI
Diagnosis of Alzheimer's Disease
TL;DR: The purpose of the meeting was to identify the most important scientific research opportunities and the crucial clinical and technical issues that influence the progress of research on the diagnosis of AD.
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The Lewy body variant of Alzheimer's disease A clinical and pathologic entity
L. A. Hansen,David P. Salmon,Douglas Galasko,Eliezer Masliah,Robert Katzman,Richard DeTeresa,Leon J. Thal,Mary Pay,Richard Hofstetter,Melville R. Klauber,Valerie A. Rice,Nelson Butters,M. Alford +12 more
TL;DR: The patients with LBs appeared to constitute a distinct neuropathologic and clinical subset of AD, the Lewy body variant (LBV), and there was an increase in essential tremor, bradykinesia, mild neck rigidity, and slowing of rapid alternating movements in the LBV group.
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An in vivo model for the neurodegenerative effects of beta amyloid and protection by substance P.
TL;DR: Beta amyloid is a potent neurotoxin in the adult brain in vivo, and its effects can be blocked by substance P, which prevented beta-amyloid-induced neuronal loss and expression of Alz-50 proteins when coadministered into the cerebral cortex.
Journal ArticleDOI
Monoclonal antibodies distinguish several differentially phosphorylated states of the two largest rat neurofilament subunits (NF-H and NF-M) and demonstrate their existence in the normal nervous system of adult rats.
TL;DR: Two-dimensional gel analysis and immunoblotting of total proteins from adult rat dorsal root ganglion verified mAb specificity in situ, and showed that differentially phosphorylated isoforms of NF-M and NF-H occur in vivo.
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Parkinson disease, dementia, and alzheimer disease: Clinicopathological correlations
TL;DR: The cerebral cortex showed senile plaques and fibrillary tangles in 15 of the 36 patients (42%) and these changes were found in all 9 patients with severe dementia, in 3 of the 7 with mild dementia, and in 2 of the 13 patients with normal mental status.
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