Unmasking the Secret Identity of p53 Protein in Alzheimer’s Disease

Published on April 28, 2022

Understanding Alzheimer’s disease is like uncovering clues to solve a mysterious crime. Scientists have proposed different theories, like the Amyloid and Tau hypotheses, to explain the puzzle. Now, there’s another suspect in the spotlight: the p53 protein. Known as a guardian of our genetic information, p53 may have a key role in the early stages of Alzheimer’s. To understand its involvement, we need to look at how p53 can change its behavior through post-translational modifications (PTMs). These modifications can alter p53’s shape and function, potentially affecting brain processes relevant to Alzheimer’s development. By studying these PTMs, scientists hope to find more targeted therapies for this debilitating disease and bring relief to countless patients.

Our understanding of Alzheimer’s disease (AD) pathogenesis has developed with several hypotheses over the last 40 years, including the Amyloid and Tau hypotheses. More recently, the p53 protein, well-known as a genome guardian, has gained attention for its potential role in the early evolution of AD. This is due to the central involvement of p53’s in the control of oxidative stress and potential involvement in the Amyloid and Tau pathways. p53 is commonly regulated by post-translational modifications (PTMs), which affect its conformation, increasing its capacity to adopt multiple structural and functional states, including those that can affect brain processes, thus contributing to AD development. The following review will explore the impact of p53 PTMs on its function and consequential involvement in AD pathogenesis. The greater understanding of the role of p53 in the pathogenesis of AD could result in more targeted therapies benefiting the many patients of this debilitating disease.

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