Tau Protein in Treating AD

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Name Professor Course Date Word Count = 1090 Advances in the Understanding and Management of Alzheimer's Disease: Tau-based therapies for Alzheimer’s disease Alzheimer's disease (AD) is recognized as the most prevalent form of dementia among older adults. With approximately 55 million individuals affected by dementia worldwide, this number is expected to rise to 139 million due to the aging population (Conti Filho et al., 2023). The global effect of Alzheimer's disease presents major problems for healthcare institutions, carers, and society at large. Significant progress has been achieved in the development of tau- based medicines for Alzheimer's disease in the quest of viable treatments. Tau protein, a microtubule-associated protein, is essential for the integrity and function of neuronal cells. However, in AD, abnormal accumulation of tau protein leads to the formation of neurofibrillary tangles and subsequent neuronal dysfunction (Sayas, 2020). The study of tau protein and its structure is essential for understanding the pathological mechanisms of AD and exploring potential therapeutic interventions. Tau-based therapies target various aspects of tau pathology, including the reduction of tau protein levels, prevention of tau aggregation, and clearance of existing tau aggregates. This new area of study has potential for the development of novel

therapeutic techniques that can alter the course of Alzheimer's disease and enhance patients' quality of life. From a therapy standpoint, it is critical to examine the Tau protein and its structure. Tau protein is located largely in the central nervous system and plays an important role in the stabilization of microtubules, which are essential for the structure and transport of neuronal cells. However, in Alzheimer's disease (AD), the aggregation of Tau protein into neurofibrillary tangles is a hallmark pathology (Sayas, 2020). Neurofibrillary tangles, along with amyloid-β plaques, are the two main pathological features associated with AD. These abnormal protein accumulations disrupt the normal functioning of neurons, leading to cognitive decline and neurodegeneration. Notably, protein aggregation is a recurring characteristic observed in AD as well as other neurodegenerative diseases. Researchers have focused on understanding the variations in the three-dimensional structure of the Tau protein to decipher its role in AD progression. Conformationally misfolded Tau protein creates toxic aggregates that spread in a prion- like fashion, leading to the development and progression of AD disease (Sayas, 2020). The spread of Tau disease worsens cognitive impairment and neuronal death in afflicted people. By gaining insights into the underlying mechanisms of Tau protein aggregation and its impact on AD pathogenesis, researchers have identified potential therapeutic targets for the development of tau-based therapies. These therapies aim to intervene in the abnormal aggregation of Tau protein and restore its normal function, thereby providing a potential avenue for managing AD. Tau-based therapies have emerged as a promising avenue for the treatment of Alzheimer's disease (AD). One Tau therapeutic approach is tau passive immunotherapy, where researchers have developed several passive vaccines that target different conformations or epitopes of Tau

protein (Conti Filho et al., 2023). These vaccines aim to promote the clearance of abnormal Tau aggregates and reduce their detrimental effects on neuronal function. Active immunotherapy is another treatment approach that includes boosting the immune system to create antibodies against the Tau protein. This technique has showed promise in preclinical investigations by increasing Tau pathology clearance and lowering cognitive impairments. In recent years, antisense treatments for tauopathies have increasingly gained consideration. Researchers now have a better grasp of the genetic elements of Tau protein, which has led to a better understanding of the function of Tau abnormalities in neurodegeneration (Jadhav et al., 2019). Antisense oligonucleotides (ASOs) and small interfering RNAs (siRNAs) have been investigated as potential therapeutic agents to reduce the production of abnormal Tau protein and halt its aggregation. The inhibition of Tau phosphorylation has as well been explored as a therapeutic strategy. Tau protein contains numerous phosphorylation sites, and abnormal phosphorylation is associated with Tau aggregation and neurofibrillary tangle formation. By targeting enzymes responsible for Tau phosphorylation, such as kinases, researchers aim to prevent or reduce Tau pathology (Soeda & Takashima, 2020). These approaches provide a diverse approach to addressing the complicated pathophysiology of Alzheimer's disease, and they show promise for the development of successful therapeutics. However, extensive preclinical and clinical research is required to evaluate their efficacy and safety in order to assure their potential translation into clinical practice. Recent advancements in tau-based therapies have shown promising results in preclinical studies and experimental findings. Researchers have focused on exploring various approaches to target tau protein and its pathological modifications, aiming to alleviate the burden of Alzheimer's disease (AD). One area of interest is focusing on other tau post-translational

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modifications, such as lysine acetylation, which modifies tau post-translationally (Medina, 2018). Understanding these modifications is crucial for designing targeted interventions to counteract their adverse effects on tau aggregation and neuronal dysfunction. To maintain an inclining trend of progress, researchers have devoted significant efforts to preclinical studies and experimental findings. These studies have provided valuable insights into the effectiveness and safety of tau-based therapies, paving the way for potential clinical applications. There is an increasing interest in combining tau-based therapy techniques with other treatment modalities. Combining tau-targeted medicines with other AD-related pathogenic processes, such as amyloid-β clearance or neuroinflammation, may provide a more holistic therapeutic strategy. Tau-based therapeutics represent a viable path for controlling AD and addressing the critical need for effective treatments. Researchers are getting closer to identifying possible breakthroughs in AD therapies by expanding their understanding of tau protein and its pathogenic activities. To sum it all, the understanding and management of Alzheimer's disease (AD) have witnessed significant advancements in tau-based therapies. Tau protein, with its crucial role in maintaining neuronal function, has emerged as a key target for intervention in AD pathology. Abnormal aggregation of tau protein into neurofibrillary tangles contributes to cognitive decline and neurodegeneration in AD. Tau-based therapeutic approaches, such as passive and active immunotherapy, antisense therapies, and inhibition of tau phosphorylation, hold promise in mitigating tau pathology and potentially slowing down disease progression. These therapeutic strategies aim to reduce the accumulation of abnormal tau aggregates, clear existing pathology, and restore neuronal function. Recent developments in tau-based therapies have explored additional tau post-translational modifications, such as lysine acetylation, and have focused on

the combination of tau-targeted approaches with other treatment modalities. These advancements are crucial in broadening the scope of potential treatment strategies for AD and addressing the multifactorial nature of the disease. Moving forward, it is critical to address the issues and obstacles that have arisen in the field of tau-based therapeutics. To confirm the effectiveness, safety, and long-term impacts of various treatment methods, rigorous preclinical and clinical studies are required. The complexities of tau disease demand more study to identify novel targets and improve existing therapy techniques.

References Conti Filho, C. E., Loss, L. B., Marcolongo-Pereira, C., Rossoni Junior, J. V., Barcelos, R. M., Chiarelli-Neto, O., ... & Mezzomo, N. J. (2023). Advances in Alzheimer’s disease’s pharmacological treatment. Frontiers in Pharmacology , 14 , 1101452. Jadhav, S., Avila, J., Schöll, M., Kovacs, G. G., Kövari, E., Skrabana, R., ... & Zilka, N. (2019). A walk through tau therapeutic strategies. Acta neuropathologica communications , 7 (1), 1-31. Medina, M. (2018). An overview on the clinical development of tau-based therapeutics. International journal of molecular sciences , 19 (4), 1160. Sayas, C. L. (2020). Tau-based therapies for Alzheimer’s disease: Promising novel neuroprotective approaches. In Neuroprotection in Autism, Schizophrenia and Alzheimer's Disease (pp. 245-272). Academic Press. Soeda, Y., & Takashima, A. (2020). New insights into drug discovery targeting tau protein. Frontiers in Molecular Neuroscience , 13 , 590896.

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