Ubiquitin-positive astrogliopathy clinically mimicking Parkinson’s disease


Journal article


Meaghan Morris, A. Moghekar, Haidan Guo, O. Pletnikova, Javier Redding-Ochoa, Marilyn Albert, S. Resnick, Liam Chen
Acta Neuropathologica Communications, 2022

Semantic Scholar DOI PubMedCentral PubMed
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APA   Click to copy
Morris, M., Moghekar, A., Guo, H., Pletnikova, O., Redding-Ochoa, J., Albert, M., … Chen, L. (2022). Ubiquitin-positive astrogliopathy clinically mimicking Parkinson’s disease. Acta Neuropathologica Communications.


Chicago/Turabian   Click to copy
Morris, Meaghan, A. Moghekar, Haidan Guo, O. Pletnikova, Javier Redding-Ochoa, Marilyn Albert, S. Resnick, and Liam Chen. “Ubiquitin-Positive Astrogliopathy Clinically Mimicking Parkinson’s Disease.” Acta Neuropathologica Communications (2022).


MLA   Click to copy
Morris, Meaghan, et al. “Ubiquitin-Positive Astrogliopathy Clinically Mimicking Parkinson’s Disease.” Acta Neuropathologica Communications, 2022.


BibTeX   Click to copy

@article{meaghan2022a,
  title = {Ubiquitin-positive astrogliopathy clinically mimicking Parkinson’s disease},
  year = {2022},
  journal = {Acta Neuropathologica Communications},
  author = {Morris, Meaghan and Moghekar, A. and Guo, Haidan and Pletnikova, O. and Redding-Ochoa, Javier and Albert, Marilyn and Resnick, S. and Chen, Liam}
}

Abstract

Several neurodegenerative pathologies can clinically mimic Parkinson’s disease, including neurodegenerative diseases with glial pathology. However, the glial aggregates are typically composed of known pathogenic proteins and are associated with prominent neuronal loss in the substantia nigra. Here we present an unusual case of a 91-year-old man with a clinical diagnosis of Parkinson’s disease, but whose autopsy findings showed a ubiquitin-positive astrogliopathy without significant neuronal loss in the substantia nigra. These glial aggregates affected the basal ganglia, cortex, and cerebellum, and were negative for tau, alpha-synuclein, TDP-43, FUS, and p62. This case is a rare example of an unknown glial neurodegenerative pathology mimicking Parkinson’s disease without significant loss of nigral dopaminergic neurons.



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