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FTLD-tau is characterised by tau positive inclusion bodies often referred to as Pick-bodies. [4] Examples of FTLD-tau include; Pick's disease, corticobasal degeneration, progressive supranuclear palsy. FTLD-TDP (or FTLD-U ) is characterised by ubiquitin and TDP-43 positive, tau negative, FUS negative inclusion bodies. The pathological histology ...
The only other known autosomal dominant genetic cause of FTLD-tau is a hypomorphic mutation in VCP which is associated with a unique neuropathology called vacuolar tauopathy. [35] FTD caused by FTLD-TDP43 has numerous genetic causes. Some cases are due to mutations in the GRN gene, also located on chromosome 17.
Alternatively, diseases exhibiting tau pathologies attributed to different and varied underlying causes are termed 'secondary tauopathies'. Some neuropathologic phenotypes involving tau protein are Alzheimer's disease, frontotemporal dementia, progressive supranuclear palsy, and corticobasal degeneration. [1]
Tau in brain of patients with tauopathies is hyperphosphorylated which causes the tau protein to dissociate from the microtubule then aggregate in to β-plated sheet arrangement. [12] PART cases is due to tau protein isoforms (3 and 4 microtubule binding repeats) abnormal ration inneural cells resulting in their self assembling and accumulation ...
SD is a clinically defined syndrome but is associated with predominantly temporal lobe atrophy (left greater than right) and hence is sometimes called temporal variant FTLD (tvFTLD). [7] SD is one of the three variants of primary progressive aphasia (PPA), which results from neurodegenerative disorders such as FTLD or Alzheimer's disease .
Many causes of dementia are neurodegenerative, and protein misfolding is a cardinal feature of these. [66] Other common causes include vascular dementia, dementia with Lewy bodies, frontotemporal dementia, and mixed dementia (commonly Alzheimer's disease and vascular dementia).
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The main known risk factor is age. Mutations in genes such as α-synuclein (SNCA), leucine-rich repeat kinase 2 (LRRK2), glucocerebrosidase (GBA), and tau protein (MAPT) can also cause hereditary PD or increase PD risk. [27] While PD is the second most common neurodegenerative disorder, problems with diagnoses still persist. [28]