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Oligodendrocytes are a Novel Source of Amyloid Peptide Generation | Neurochemical Research
Description:
Alzheimer’s disease is characterised by regional neuronal degeneration, synaptic loss, and the progressive deposition of the 4 kDa β-amyloid peptide (Aβ) in senile plaques and accumulation of tau protein as neurofibrillary tangles. Aβ derives from the larger precursor molecule, amyloid precursor protein (APP) by proteolytic processing via β- and γ-secretases. While APP expression is well documented in neurons and astrocytes, the case for oligodendrocytes is less clear. The latter cell type is reported to express different isoforms of APP, and we have confirmed this observation by immunocytochemistry in cultures of differentiated rat cortical oligodendrocytes. Moreover, by means of a sensitive electrochemiluminescent immunoassay employing Aβ C-terminal specific antibodies, mature oligodendrocytes are shown to secrete the 40 and 42 amino acid Aβ species (Aβ40 and Aβ42). Secretion of Aβ peptides was reduced by incubating oligodendrocytes with α- and β-secretase inhibitors, or a γ-secretase inhibitor. Disturbances of APP processing and/or synthesis in oligodendrocytes may account for some myelin disorders observed in Alzheimer’s disease and other senile dementias.
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article, google, scholar, pubmed, cas, amyloid, alzheimers, disease, protein, precursor, neurosci, oligodendrocytes, brain, res, cell, βamyloid, expression, rat, nature, research, peptide, skaper, neurochem, app, βsecretase, inhibitor, selkoe, neuron, bace, privacy, cookies, content, processing, cells, mice, localization, beta, protease, publish, search, june, stephen, evans, rosin, neuronal, senile, plaques, peptides, access, sci,
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month download article/chapter 4 kda β-amyloid peptide aβ oligomer-induced aberrations amyloid β-protein precursor β-amyloid precursor protein beta-amyloid precursor protein neutral sphingomyelinase-ceramide pathway amyloid peptide generation amyloid-β production age-related myelin breakdown disease neurodegeneration access disease-related cognitive deficits x-ray diffraction evidence a4 amyloid mrna age-related cognitive decline β-amyloid reductions amyloid β-protein full article pdf amyloid-β peptides β-secretase cleavage garcía-ladona fj amyloid precursor protein cerebrovascular amyloid protein privacy choices/manage cookies beta amyloid toxicity cultured neural cells clonal neural cells amyloid-β plaques β-secretase bace1 naturally secreted oligomers selkoe dj kunitz protease inhibitor β-secretase inhibitors γ-secretase inhibitor cell-permeant inhibitor x-ray structure larger precursor molecule cerebral amyloid angiopathy peripheral nervous system protease nexin-ii disease amyloid hypothesis conditions privacy policy senile plaque amyloid mice affects remyelination peripheral nervous systems related subjects european economic area myelin disorders observed paired helical filament subcortical arteriosclerotic encephalopathy
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headline:Oligodendrocytes are a Novel Source of Amyloid Peptide Generation
description:Alzheimer’s disease is characterised by regional neuronal degeneration, synaptic loss, and the progressive deposition of the 4 kDa β-amyloid peptide (Aβ) in senile plaques and accumulation of tau protein as neurofibrillary tangles. Aβ derives from the larger precursor molecule, amyloid precursor protein (APP) by proteolytic processing via β- and γ-secretases. While APP expression is well documented in neurons and astrocytes, the case for oligodendrocytes is less clear. The latter cell type is reported to express different isoforms of APP, and we have confirmed this observation by immunocytochemistry in cultures of differentiated rat cortical oligodendrocytes. Moreover, by means of a sensitive electrochemiluminescent immunoassay employing Aβ C-terminal specific antibodies, mature oligodendrocytes are shown to secrete the 40 and 42 amino acid Aβ species (Aβ40 and Aβ42). Secretion of Aβ peptides was reduced by incubating oligodendrocytes with α- and β-secretase inhibitors, or a γ-secretase inhibitor. Disturbances of APP processing and/or synthesis in oligodendrocytes may account for some myelin disorders observed in Alzheimer’s disease and other senile dementias.
datePublished:2009-06-26T00:00:00Z
dateModified:2009-06-26T00:00:00Z
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Oligodendrocytes
Amyloid peptides
Secretases
Cortex
Alzheimer’s disease
Neurodegeneration
Neurosciences
Neurochemistry
Biochemistry
general
Cell Biology
Neurology
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headline:Oligodendrocytes are a Novel Source of Amyloid Peptide Generation
description:Alzheimer’s disease is characterised by regional neuronal degeneration, synaptic loss, and the progressive deposition of the 4 kDa β-amyloid peptide (Aβ) in senile plaques and accumulation of tau protein as neurofibrillary tangles. Aβ derives from the larger precursor molecule, amyloid precursor protein (APP) by proteolytic processing via β- and γ-secretases. While APP expression is well documented in neurons and astrocytes, the case for oligodendrocytes is less clear. The latter cell type is reported to express different isoforms of APP, and we have confirmed this observation by immunocytochemistry in cultures of differentiated rat cortical oligodendrocytes. Moreover, by means of a sensitive electrochemiluminescent immunoassay employing Aβ C-terminal specific antibodies, mature oligodendrocytes are shown to secrete the 40 and 42 amino acid Aβ species (Aβ40 and Aβ42). Secretion of Aβ peptides was reduced by incubating oligodendrocytes with α- and β-secretase inhibitors, or a γ-secretase inhibitor. Disturbances of APP processing and/or synthesis in oligodendrocytes may account for some myelin disorders observed in Alzheimer’s disease and other senile dementias.
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Oligodendrocytes
Amyloid peptides
Secretases
Cortex
Alzheimer’s disease
Neurodegeneration
Neurosciences
Neurochemistry
Biochemistry
general
Cell Biology
Neurology
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