Journal
BRAIN PATHOLOGY
Volume 17, Issue 1, Pages 74-82Publisher
WILEY
DOI: 10.1111/j.1750-3639.2007.00054.x
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Funding
- NIA NIH HHS [P50 AG016574, P01-AG14449, R01 AG015866, P50-AG16574, P01 AG014449, P01-AG17216, P01-AG03949, R01-AG15866, P01 AG003949, P50-AG25711, P01 AG017216, P50 AG025711] Funding Source: Medline
- NIEHS NIH HHS [R01 ES013941, R01-ES02941] Funding Source: Medline
- NINDS NIH HHS [P50 NS040256, P01 NS040256, P50-NS40256] Funding Source: Medline
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [P50NS040256] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [P01AG017216, P01AG014449, R01AG015866, P50AG025711, P01AG003949, P50AG016574] Funding Source: NIH RePORTER
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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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