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IJSTR >> Volume 10 - Issue 11, November 2021 Edition



International Journal of Scientific & Technology Research  
International Journal of Scientific & Technology Research

Website: http://www.ijstr.org

ISSN 2277-8616



The Role Of Tau In The Onset And Progression Of Alzheimer’s Disease Within The Cyclical Immunoreactive Theory Of AD

[Full Text]

 

AUTHOR(S)

Peter Iacobelli

 

KEYWORDS

Alzheimer’s, Tau, Proteins, Neurodegeneration, Neuroscience, Neuropathology

 

ABSTRACT

The causal mechanism from which Alzheimer’s Disease (AD) originates has yet to be illuminated in full, although significant progress has been made in that very direction. Ideas have been put forth since the disease’s founding by Dr. Alois Alzheimer over 100 years ago that have implicated the beta amyloid (Aβ) peptide in the onset and progression of the disease in its exclusively elderly population of patients, as aggregations of this antimicrobial protein formed plaques in the autopsied brain of the earliest studied AD brain and in all of those that have come after her. Because increased availability of improved technology has allowed for greater observational tracing of the disease, it has come to be known that the quantity of Aβ deposition is directly proportional to the severity of the behavioral symptoms observed of the patient in question. This left little doubt as to whether or not Aβ played an important role in the exacerbation of AD, and it is on these grounds that ideas such as the common amyloid cascade hypothesis have been put forth. While incomplete, these long standing frameworks for thinking about the intricacies and causal mechanisms of AD have given way to more complete theories on the matter such as the cyclical immunoreactive theory of AD. Nonetheless, all plausible frameworks surrounding the onset and progression of AD afford the majority of their focus to Aβ, while ignoring some of the more peripheral, though important elements of AD. Perhaps the only rival to Aβ in terms of prevalence, consistent presence, and potential causal involvement is the tau protein. Having also been observed very early on in the autopsied brains of AD patients by Dr. Alzheimer the microtubule associated protein (MAP) tau has been shown to aggregate in a manner similar to that of Aβ in the AD brain. These accumulations of the pathological protein are called neurofibrillary tangles (NFTs), and no doubt play a role similar to Aβ plaques in the slow yet consistent progression of the neurodegenerative disease. This text will assess the role of the tau protein in the brain of AD patients, and review relevant studies on the subject all with the aim of defining its role within the context of what is thus far the most complete framework for diagnosing and describing the intricacies of AD.

 

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