Abstract

Neurodegenerative diseases like Alzheimer’s disease (AD) are poised to become a global health crisis, and therefore understanding the mechanisms underlying the pathogenesis is critical for the development of therapeutic strategies. Mutations in genes encoding presenilin (PSEN) occur in most familial Alzheimer’s disease but the role of PSEN in AD is not fully understood. In this review, the potential modes of pathogenesis of AD are discussed, focusing on calcium homeostasis and mitochondrial function. Moreover, research using Caenorhabditis elegans to explore the effects of calcium dysregulation due to presenilin mutations on mitochondrial function, oxidative stress and neurodegeneration is explored.

Highlights

  • As baby boomers enter retirement age, there could be a potential global health crisis due to the occurrence of various neurodegenerative diseases

  • The brain is highly susceptible to oxidative stress due its increased energy demand and high rates of metabolism, which when left unchecked can result in neurodegeneration

  • We explore the role of mitochondrial dysfunction and oxidative stress in Alzheimer’s disease

Read more

Summary

Introduction

As baby boomers enter retirement age, there could be a potential global health crisis due to the occurrence of various neurodegenerative diseases. Alzheimer’s disease (AD) poses the greatest threat due to its prevalence, the lack of a clear understanding of its pathogenesis and inefficiency of current therapeutic strategies. Oxidative stress occurs due to a disparity in redox states brought on by either an excessive generation of reactive oxygen species (ROS) or a reduction in antioxidant function. As the site of ROS production and breakdown, the mitochondria play a critical role in controlling oxidative stress and mitochondrial dysfunction can be detrimental to organismal health. Understanding the role of ROS in neurodegenerative diseases like AD could provide much needed insight into the development of novel therapeutic targets. We explore the role of mitochondrial dysfunction and oxidative stress in Alzheimer’s disease

Mitochondria
Alzheimer’s Disease
Presenilin and the Calcium Hypothesis of Alzheimer’s Disease
Oxidative Stress Mediated Neurodegeneration in sel-12 Mutants
Presenilin and γ-Secretase Function
Findings
11. Future Directions and Conclusions
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call