Amyloid-β peptide (Aβ) and tau protein deposits in the human brain are the pathological hallmarks of Alzheimer’s disease (AD). Tau is a class of proteins that are abundant in nerve cells and perform the function of stabilizing microtubules. However, in certain pathological situations, Tau proteins become defective and fail to adequately stabilize microtubules, which can result in the generation of abnormal masses that are toxic to neurons. This process occurs in a number of neurological disorders collectively known as Tauopathies. Tau protein is the major factor of the intracellular filamentous deposits that relate to a number of neurodegenerative diseases which includes the progressive supranuclear palsy (PSP), Pick’s disease, and Parkinsonism. The identification of mutations in Tau established that dysfunction or misregulation of tau protein is sufficient to cause dementia and neurodegeneration. In this review article, we discussed the etiology of the tau formation and role in AD and subsequently therapeutic approach for disassembling and Tau inhibition.