[1] Hyperphosphorylation of tau proteins causes them to dissociate from microtubules and form insoluble aggregates called neurofibrillary tangles.

[2] Various neuropathologic phenotypes have been described based on the anatomical regions and cell types involved as well as the unique tau isoforms making up these deposits.

Some neuropathologic phenotypes involving tau protein are Alzheimer's disease, frontotemporal dementia, progressive supranuclear palsy, and corticobasal degeneration.

Variants of Tau isoforms, spanning from 352 to 441 amino acids, arise through the alternative splicing of exons 2,3 and 10 within the MAPT gene.

[3] Positron emission tomography (PET) is one type of biomarker capable of identifying elevated levels of tau in patients with Alzheimer's disease.

Substantial data on CSF biomarkers is available for Alzheimer's disease (AD), focusing on measures related to total and phosphorylated forms of tau and amyloid-beta (Aβ) protein.

[6] Alzheimer's disease (AD) is clinically characterized by a progressive decline in memory and cognitive functions, leading to severe dementia.

[7][8] Nevertheless, AD neurofibrillary lesions were the first to undergo ultrastructural and biochemical analysis, thus laying the foundation for in-depth studies on tau protein deposition in various tauopathies.