Co-localization of α-synuclein and phosphorylated tau in neuronal and glial cytoplasmic inclusions in a patient with multiple system atrophy of long duration

@article{Piao2000ColocalizationO,
  title={Co-localization of $\alpha$-synuclein and phosphorylated tau in neuronal and glial cytoplasmic inclusions in a patient with multiple system atrophy of long duration},
  author={Yueshan Piao and Shintaro Hayashi and Masato Hasegawa and Koichi Wakabayashi and Mitsunori Yamada and Makoto Yoshimoto and Atsushi Ishikawa and Takeshi Iwatsubo and Hitoshi Takahashi},
  journal={Acta Neuropathologica},
  year={2000},
  volume={101},
  pages={285-293}
}
Abstract. Neuronal and glial cytoplasmic inclusions (NCIs and GCIs), which contain α-synuclein as a major component, are characteristic cytopathological features of multiple system atrophy (MSA). We report MSA of 19 years' duration in a 73-year-old woman. Her initial symptom was parkinsonism, with dementia appearing about 8 years later. Postmortem examination showed marked atrophy of the frontal and temporal white matter and limbic system, in addition to the pathology typical of MSA. In the… 
Progressive accumulation of ubiquitin and disappearance of α-synuclein epitope in multiple system atrophy-associated glial cytoplasmic inclusions: triple fluorescence study combined with Gallyas-Braak method
TLDR
Progressive accumulation of Ub with concomitant disappearance of αS epitope and their colocalization, partly shared with LBs, may represent a process of GCI formation, possibly linked to an aspect of degeneration in MSA.
Mutant ubiquitin and p62 immunoreactivity in cases of combined multiple system atrophy and Alzheimer’s disease
TLDR
It is indicated that α-synuclein and phosphorylated tau co-occur in certain brain regions in cases of combined MSA and AD and that the proteasomal pathways differ between α- synuclein- and pTau-bearing neurons.
Tau‐positive glial cytoplasmic granules in multiple system atrophy
TLDR
Results indicate that tau‐positive granules in glia are common findings in MSA and that t Tau aggregation might be another pathway to neurodegeneration in M SA.
PATHOLOGY OF NEURO-GLIAL α-SYNUCLEINOPATHY (LEWY BODY DISEASE AND MULTIPLE SYSTEM ATROPHY)
TLDR
Two degenerative processes have been considered in Parkinsons disease with Lewy bodies and multiple system atrophy; one is due to the widespread occurrence of GCIs associated with oligodendroglia‑myelin degeneration and the other isdue to the aggregation of αS in neurons in several brain regions that might synergistically cause neuronal depletion in MSA.
Extensive distribution of glial cytoplasmic inclusions in an autopsied case of multiple system atrophy with a prolonged 18‐year clinical course
TLDR
This case had complicated hypoxic encephalopathy, but p‐α‐syn+ GCIs were also found in the damaged white matter, indicating the contribution of α‐syncleinopathy as well as hypoxic effect to the secondary myelin and axonal loss in the white matter.
Absence of α-synuclein mRNA expression in normal and multiple system atrophy oligodendroglia
TLDR
Oligodendroglia do not express α-synuclein mRNA in control and MSA cases suggesting that involvement of α- Synuclein in GCI pathology of MSA is due to its ectopic presence in oligodendrogramlia.
Accumulation of phosphorylated α‐synuclein in subpial and periventricular astrocytes in multiple system atrophy of long duration
TLDR
Immunohistochemically examined the frontal and temporal lobes, basal ganglia, cerebellum, brainstem and spinal cord of patients with MSA and Lewy body disease, and also in control subjects, and revealed that the phosphorylated α‐synuclein‐immunoreactive structures in astrocytes were non‐fibrillar and associated with granular and vesicular structures.
Perirhinal accumulation of neuronal alpha‐synuclein in a multiple system atrophy patient with dementia
  • M. Saito, M. Hara, +7 authors S. Kamei
  • Biology, Medicine
    Neuropathology : official journal of the Japanese Society of Neuropathology
  • 2017
TLDR
The case of a 79‐year‐old Japanese woman who developed cerebellar ataxia followed by rigidity, dysautonomia and cognitive disorders, and was thus clinically diagnosed as having possible MSA with dementia is reported, to provide clues to elucidate how neuronal pathology evolves in the hippocampal/parahippocampal regions in MSA, particularly in cases with dementia.
α‐Synuclein‐positive structures in association with diffuse neurofibrillary tangles with calcification
TLDR
The findings suggest that the accumulation pattern of α− Synuclein is a pathological feature of DNTC, and that DNTC is associated with accumulation of both tau and α−synuclein.
The role of α-synuclein in the pathogenesis of multiple system atrophy
TLDR
Transgenic MSA mouse models are now available to determine aspects of cellular disturbance experimentally that suggest a fundamental disturbance of the functional unit between oligodendroglia, axon, and neuron in MSA.
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TLDR
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TLDR
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