Progressive Supranuclear Palsy: Pathology and Genetics
Open accessAbstract
Progressive supranuclear palsy (PSP) is an atypical Parkinsonian disorder associated with progressive axial rigidity, vertical gaze palsy, dysarthria and dysphagia. Neuropathologically, the subthalamic nucleus and brainstem, especially the midbrain tectum and the superior cerebellar peduncle, show atrophy. The substantia nigra shows loss of pigment corresponding to nigrostriatal dopaminergic degeneration. Microscopic findings include neuronal loss, gliosis and neurofibrillary tangles in basal ganglia, diencephalon and brainstem. Characteristic tau pathology is also found in glia. The major genetic risk factor for sporadic PSP is a common variant in the gene encoding microtubule‐associated protein tau (MAPT) and recent studies have suggested that this may result in the altered expression of specific tau protein isoforms. Imaging studies suggest that there may be sensitive and specific means to differentiate PSP from other parkinsonian disorders, but identification of a diagnostic biomarker is still elusive.
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Progressive supranuclear palsy arises from the aggregation of tau protein in neuroglial cells, most prominently in the basal ganglia, diencephalon, and brainstem.
“Progressive supranuclear palsy (PSP) is a devastating neurodegenerative disorder caused by the neuro-glial aggregation of tau protein, particularly in the basal ganglia, diencephalon, and brainstem1,2.”
From Neuroinflammation and Tau Colocalize in vivo in Progressive Supranuclear Palsy (2020) · cites this paper as [1]
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“Whereas CBD pathology predominantly affects forebrain structures (including the neocortex) and midbrain structures (including the substantia nigra), PSP pathology demonstrates a predilection for affecting hindbrain regions including the tectum, tegmentum, midbrain as well as the globus pallidus and diencephalon [14, 1…”
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- Authors
- Dickson, D. W., Rademakers, R., & Hutton, M. L.
- Affiliations
- Mayo Clinic in Florida (US)
- Venue
- Brain Pathology
- Publisher
- Wiley
- Published
- 2007-01
- Volume
- 17
- Issue
- 1
- Pages
- 74-82
- ISSN
- 1015-6305 (ISSN-L)
- 1750-3639
- PMC
- PMC8095545
- OpenAlex
- W2014875179
- Cited by
- 314
- References
- 99
- Citations by year
- 2026: 20 · 2025: 24 · 2024: 25 · 2023: 25 · 2022: 15 · 2021: 17 · 2020: 11 · 2019: 18 · 2018: 7 · 2017: 25 · 2016: 19 · 2015: 11 · 2014: 17 · 2013: 14 · 2012: 10
- FWCI
- 1.58
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Brain Pathology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute on Aging (R01AG015866, P01AG014449, P01AG003949, P50AG025711, P01AG017216, P50AG016574)
- National Institute of Neurological Disorders and Stroke (P01NS040256, P50NS040256)
- National Institute of Environmental Health Sciences (R01ES013941, R01-ES02941)
- Topics
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Health Sciences › Medicine › Neurology › Neurological disorders and treatments
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Keywords
- progressive supranuclear palsy, tauopathy, tau pathology, MAPT gene, tau isoforms, atypical parkinsonism, subthalamic nucleus, midbrain tectum, superior cerebellar peduncle, nigrostriatal degeneration, neurofibrillary tangles, gliosis, brainstem atrophy, differential diagnosis, diagnostic biomarkers, neuroimaging
- MeSH terms
- Humans, Supranuclear Palsy, Progressive, tau Proteins
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