The fine structure of some intraganglionic alterations. Neurofibrillary tangles, granulovacuolar bodies and "rod-like" structures as seen in Guam amyotrophic lateral sclerosis and parkinsonism-dementia complex.
about
Ultrastructural study of Betz cells in the primary motor cortex of the human brainMammalian E4 is required for cardiac development and maintenance of the nervous system.Cytoskeletal pathologies of Alzheimer diseaseHirano bodies differentially modulate cell death induced by tau and the amyloid precursor protein intracellular domain.Neuropathology of Alzheimer's diseaseUbiquitin is associated with abnormal cytoplasmic filaments characteristic of neurodegenerative diseases.Transgenic mouse model for the formation of Hirano bodies.Cofilin expression induces cofilin-actin rod formation and disrupts synaptic structure and function in Aplysia synapses.Model Hirano bodies protect against tau-independent and tau-dependent cell death initiated by the amyloid precursor protein intracellular domain.Granulovacuolar degeneration (GVD) bodies of Alzheimer's disease (AD) resemble late-stage autophagic organelles.Ubiquitin is detected in neurofibrillary tangles and senile plaque neurites of Alzheimer disease brains.Neurofibrillary degeneration in amyotrophic lateral sclerosis/parkinsonism-dementia complex of Guam. Immunochemical characterization of tau proteins.Granular expression of prolyl-peptidyl isomerase PIN1 is a constant and specific feature of Alzheimer's disease pathology and is independent of tau, Aβ and TDP-43 pathologyFormation of Hirano bodies induced by expression of an actin cross-linking protein with a gain-of-function mutation.Tau and alpha-synuclein pathology in amygdala of Parkinsonism-dementia complex patients of GuamFree fatty acids stimulate the polymerization of tau and amyloid beta peptides. In vitro evidence for a common effector of pathogenesis in Alzheimer's disease.Early accumulation of heparan sulfate in neurons and in the beta-amyloid protein-containing lesions of Alzheimer's disease and Down's syndrome.Sequestration of tau by granulovacuolar degeneration in Alzheimer's disease.The development of the pathologic changes of Alzheimer's disease and senile dementia in patients with Down's syndrome.Subacute spongiform virus encephalopathies. Scrapie, Kuru and Creutzfeldt-Jakob disease: a review.Postsynaptic degeneration as revealed by PSD-95 reduction occurs after advanced Aβ and tau pathology in transgenic mouse models of Alzheimer's diseaseCorpora Amylacea in Neurodegenerative Diseases: Cause or Effect?Crystalline ribosomes are present in brains from senile humansCorrelation of Alzheimer disease neuropathologic changes with cognitive status: a review of the literatureImmunocytochemical characterization of glial fibrillary tangles in Alzheimer's disease brain.Systemic lupus erythematosus clinically resembling multiple sclerosis and with unusual pathological and ultrastructural features.De novo actin polymerization is required for model Hirano body formation in Dictyostelium.Progressive myoclonus and epilepsy with dentatorubral degeneration: a clinicopathological study of the Ramsay Hunt syndrome.Formation of Hirano bodies after inducible expression of a modified form of an actin-cross-linking protein.Straight and paired helical filaments in Alzheimer disease have a common structural unitCytoplasmic inclusions of TDP-43 in neurodegenerative diseases: a potential role for caspases.Paired helical filaments from Alzheimer disease patients contain cytoskeletal components.Alzheimer's disease--neuropathological aspects.Granulovacuolar Degeneration in Hippocampus of Neurodegenerative Diseases: Quantitative Study.Requirements for Hirano body formationMonoclonal antibodies to Alzheimer neurofibrillary tangles. 2. Demonstration of a common antigenic determinant between ANT and neurofibrillary degeneration in progressive supranuclear palsy.Hirano body expression impairs spatial working memory in a novel mouse model.Immunohistological study of granulovacuolar degeneration using monoclonal antibodies to neurofilaments.A Single Neonatal Exposure to BMAA in a Rat Model Produces Neuropathology Consistent with Neurodegenerative Diseases.Identification of changes in neuronal function as a consequence of aging and tauopathic neurodegeneration using a novel and sensitive magnetic resonance imaging approach.
P2860
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P2860
The fine structure of some intraganglionic alterations. Neurofibrillary tangles, granulovacuolar bodies and "rod-like" structures as seen in Guam amyotrophic lateral sclerosis and parkinsonism-dementia complex.
description
1968 nî lūn-bûn
@nan
1968 թուականի Ապրիլին հրատարակուած գիտական յօդուած
@hyw
1968 թվականի ապրիլին հրատարակված գիտական հոդված
@hy
1968年の論文
@ja
1968年論文
@yue
1968年論文
@zh-hant
1968年論文
@zh-hk
1968年論文
@zh-mo
1968年論文
@zh-tw
1968年论文
@wuu
name
The fine structure of some int ...... parkinsonism-dementia complex.
@ast
The fine structure of some int ...... parkinsonism-dementia complex.
@en
The fine structure of some int ...... parkinsonism-dementia complex.
@nl
type
label
The fine structure of some int ...... parkinsonism-dementia complex.
@ast
The fine structure of some int ...... parkinsonism-dementia complex.
@en
The fine structure of some int ...... parkinsonism-dementia complex.
@nl
prefLabel
The fine structure of some int ...... parkinsonism-dementia complex.
@ast
The fine structure of some int ...... parkinsonism-dementia complex.
@en
The fine structure of some int ...... parkinsonism-dementia complex.
@nl
P2093
P1476
The fine structure of some int ...... parkinsonism-dementia complex.
@en
P2093
Dembitzer HM
Kurland LT
Zimmerman HM
P304
P577
1968-04-01T00:00:00Z