Progressive supranuclear palsy (PNP) is a neurodegenerative disease characterized by a combination of progressive akinetic-rigid syndrome, postural instability with frequent falls, supranuclear ophthalmoplegia, pseudobulbar syndrome and frontal dementia. The disease usually develops after the sixth decade of life, and has a progressive course. An own description of the clinical case of progressive supranuclear palsy in a 79-year-old patient with oromandibular hyperkinesis while taking levodopa is presented.
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Background: The hyperphosphorylation, mislocalization, and aggregation of the microtubule associated protein Tau (MAPT) is a driving force in tauopathies, a group of progressive, neurodegenerative disorders. These pathogenic intracellular aggregates, known as neurofibrillary tangles (NFTs), are a hallmark in several diseases such as frontotemporal dementia, progressive supranuclear palsy, and Alzheimer's Disease. While anti-Tau immunotherapies emphasize the clearance of extracellular Tau aggregates, they do not address the intracellular accumulation of NFTs.
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