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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.
Frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17) is an autosomal dominant neurodegenerative tauopathy and Parkinson plus syndrome. [3] FTDP-17 is caused by mutations in the MAPT (microtubule associated protein tau) gene located on the q arm of chromosome 17, and has three cardinal features: behavioral and personality changes, cognitive impairment, and motor symptoms.
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 ...
[12] [17] [18] Detachment of tau from microtubules causes the neuron to lose its ability to sustain itself and thus ultimately it loses function. Hyper-phosphorylation of tau protein was initially thought to be caused by Aβ 42 but since PART cases generally lack senile plaques, other causes were investigated. One such cause was found to me the ...
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 .
In some cases, dry macular degeneration can convert to “wet” degeneration, caused by “bleeding or a leaky blood vessel,” that leads to a much more rapid loss of visual acuity, explains ...
Alzheimer's disease (AD) is a chronic neurodegenerative disease that results in the loss of neurons and synapses in the cerebral cortex and certain subcortical structures, resulting in gross atrophy of the temporal lobe, parietal lobe, and parts of the frontal cortex and cingulate gyrus. [14]
In Alzheimer's disease, tau undergoes chemical changes, becoming hyperphosphorylated; it then begins to pair with other threads, creating neurofibrillary tangles and disintegrating the neuron's transport system. [107] Pathogenic tau can also cause neuronal death through transposable element dysregulation. [108]