Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1007/s00401-006-0075-7 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
SNCA and TPPP transcripts increase in oligodendroglial cytoplasmic inclusions in multiple system atrophy.
Neurobiol Dis
August 2024
Tanz Centre for Research in Neurodegenerative Disease, University of Toronto, Toronto, ON, Canada; Dementia Research Centre, Macquarie Medical School, Faculty of Medicine, Health and Human Sciences, Macquarie University, Sydney, Australia; Laboratory Medicine Program and Krembil Brain Institute, University Health Network, Toronto, ON, Canada; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, Canada; Edmund J Safra Program in Parkinson's Disease and Rossy Progressive Supranuclear Palsy Centre, Toronto Western Hospital, Toronto, ON, Canada; Department of Medicine, Division of Neurology, University of Toronto, Toronto, ON, Canada. Electronic address:
Multiple system atrophy (MSA) is characterized by glial cytoplasmic inclusions (GCIs) containing aggregated α-synuclein (α-syn) in oligodendrocytes. The origin of α-syn accumulation in GCIs is unclear, in particular whether abnormal α-syn aggregates result from the abnormal elevation of endogenous α-syn expression in MSA or ingested from the neuronal source. Tubulin polymerization promoting protein (TPPP) has been reported to play a crucial role in developing GCI pathology.
View Article and Find Full Text PDFShared and Distinct Patterns of Oligodendroglial Response in α-Synucleinopathies and Tauopathies.
J Neuropathol Exp Neurol
December 2016
From the Department of Pathology and Molecular Medicine, Thomayer Hospital, Prague, Czech Republic (ZR, RM), Institute of Neurology, Medical University of Vienna, Vienna, Austria (IM, MIL, GGK), and Institute of Pathology of the First Faculty of Medicine of Charles University in Prague and General Teaching Hospital, Prague, Czech Republic (RM).
Pathological protein deposits in oligodendroglia are common but variable features of various neurodegenerative conditions. To evaluate oligodendrocyte response in neurodegenerative diseases (NDDs) with different extents of oligodendroglial protein deposition we performed immunostaining for tubulin polymerization-promoting protein p25α (TPPP/p25α), α-synuclein (α-syn), phospho-tau, ubiquitin, myelin basic protein, and the microglial marker HLA-DR. We investigated cases of multiple system atrophy ([MSA] n = 10), Lewy body disease ([LBD] n = 10), globular glial tauopathy ([GGT] n = 7) and progressive supranuclear palsy ([PSP] n = 10).
View Article and Find Full Text PDFp25α/tubulin polymerization promoting protein (TPPP) is an oligodendroglial protein that plays crucial roles including myelination, and the stabilization of microtubules. In multiple system atrophy (MSA), TPPP is suggested to relocate from the myelin sheath to the oligodendroglial cell body, before the formation of glial cytoplasmic inclusions (GCIs), the pathologic hallmark of MSA. However, much is left unknown about the re-distribution of TPPP in MSA.
View Article and Find Full Text PDFp25alpha relocalizes in oligodendroglia from myelin to cytoplasmic inclusions in multiple system atrophy.
Am J Pathol
October 2007
Prince of Wales Medical Research Institute, Randwick, New South Wales, Australia.
p25alpha is an oligodendroglial protein that can induce aggregation of alpha-synuclein and accumulates in oligodendroglial cell bodies containing fibrillized alpha-synuclein in the neurodegenerative disease multiple system atrophy (MSA). We demonstrate biochemically that p25alpha is a constituent of myelin and a high-affinity ligand for myelin basic protein (MBP), and in situ immunohistochemistry revealed that MBP and p25alpha colocalize in myelin in normal human brains. Analysis of MSA cases reveals dramatic changes in p25alpha and MBP throughout the course of the disease.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!