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Diseases known to present with these aggregates are termed tauopathies, of which the most well-known is AD. The tau protein stabilizes microtubules in neurons, but abnormal hyperphosphorylation of tau leads to aggregate formation. More recently, however, the tau hypothesis has gained traction. Initially, the Aβ theory prevailed against the tau theory, especially as mutations were identified in the amyloid precursor protein located on chromosome 21 that corresponds to amyloid build-up and AD phenotypes. The hallmarks of AD are largely twofold: insoluble deposits of Aβ located between neurons and clumps of NFTs composed of tau aggregates found within nerve cells. The cholinergic hypothesis states that low production of acetylcholine (ACh) initiates AD, while the observation of Aβ and NFTs lead to the amyloid and tau hypotheses as causes for AD development. Several hypotheses have been proposed to explain the onset and development of AD. Since Alois Alzheimer described the disease, its cause remains unknown except for less than 5% of the cases that are genetic, with mutations observed in amyloid precursor protein, presenilin-1 and -2, displaying autosomal-dominant familial AD, and in the autosomal-recessive AD apolipoprotein E-e4 ( ApoE4). As the disease progresses, AD patients withdraw more and more from work and social activities to depend on total care from caregivers. The observed symptoms for AD are related to cognitive decline, memory loss, confusion, problems with reading, writing and speaking, along with changes in mood and personality. Alzheimer’s disease (AD) was first described in 1906 by Aloysius ‘Alois’ Alzheimer, a German psychiatrist and neuropathologist who identified and described amyloid plaques (Aβ) and neurofibrillary tangles (NFTs) from a 51-year old patient named Auguste Deter who showed strangely impaired behavior.