Abstract
Progressive supranuclear palsy (PSP) is an adult-onset neurodegenerative disease, clinically characterized by prominent postural instability and falls, vertical supranuclear gaze palsy, and frontal-subcortical dementia. The etiology is still unknown but recent scientific advances have led to a consensus that the main pathogenetic event is the abnormal 4R tau deposition in the brainstem, basal ganglia, and neocortical areas. The clinical spectrum has been expanded and includes several clinical syndromes that can be underpinned by the pathological hallmark features of PSP. Attempts to identify a biomarker in the cerebrospinal fluid or a specific and sensitive neuroimaging technique have so far failed to contribute significantly to the diagnostic process. Symptomatic pharmacologic treatment of PSP is still unsatisfactory, and the effect of dopaminergic medication on the parkinsonian symptoms is limited. Although the first disease-modifying trials have failed to show any clinical benefit, they have signaled the beginning of a new era towards finding an effective treatment for this devastating disorder.
The updated online version of the original chapter can be found under DOI 10.1007/978-3-7091-1628-9_18
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Fig. 18.1 Tau pathology in a postmortem brain of a PSP patient within the basal ganglia. Immunostaining with the AD2 antibody against human tau. Pathological AD2 immunoreaction in cytoplasm of oligodendrocytes (coiled body) and astrocytes (tuff), in neurites (threads), and in neuronal cytoplasm in loose (pre-tangle) and dense aggregation (tangle) (Stamelou et al, 2010) (Photos: G. Hoeglinger)
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Stamelou, M., Oertel, W.H. (2017). Erratum to: Progressive Supranuclear Palsy. In: Falup-Pecurariu, C., Ferreira, J., Martinez-Martin, P., Chaudhuri, K. (eds) Movement Disorders Curricula. Springer, Vienna. https://doi.org/10.1007/978-3-7091-1628-9_45
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DOI: https://doi.org/10.1007/978-3-7091-1628-9_45
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