Abstract

Alzheimer’s disease (AD) is a current public health challenge and will remain until the development of an effective intervention. However, developing an effective treatment for the disease requires a thorough understanding of its etiology, which is currently lacking. Although several studies have shown the association between oxidative damage and AD, only a few have clarified the specific mechanisms involved. Herein, we reviewed recent preclinical and clinical studies that indicated the significance of oxidative damage in AD, as well as potential antioxidants. Although several factors regulate oxidative stress in AD, we centered our investigation on apolipoprotein E and the gut microbiome. Apolipoprotein E, particularly apolipoprotein E-ε4, can impair the structural facets of the mitochondria. This, in turn, can minimize the mitochondrial functionality and result in the progressive build-up of free radicals, eventually leading to oxidative stress. Similarly, the gut microbiome can influence oxidative stress to a significant degree via its metabolite, trimethylamine N-oxide. Given the various roles of these two factors in modulating oxidative stress, we also discuss the possible relationship between them and provide future research directions.

Highlights

  • A progressive cognitive impairment is a significant indication of Alzheimer’s disease

  • We examined several potential antioxidants currently being explored for Alzheimer’s disease (AD)

  • The more significant finding was that 74% of the mild cognitive impairment (MCI) patients were non–apolipoprotein E (APOE)-ε4 carriers. The importance of this discovery is because the increased Superoxide dismutase (SOD) level in MCI patients relative to healthy controls might reflect the higher number of non–APOE-ε4 carriers

Read more

Summary

Introduction

A progressive cognitive impairment is a significant indication of Alzheimer’s disease (hereafter: AD). Enormous efforts have been undertaken to determine AD’s underlying causative and pathophysiological factors, these investigations have been largely inconclusive Recent studies such as the potentiality of 40-Hz light flickers as an interventional therapy and early detection of the disease via blood plasma have shown promising results [4, 5]. The latter study is appealing because it evaluated potential disease biomarkers in a large number of cognitively impaired and unimpaired individuals, with their aberrancy associated with neurodegeneration [5]. Chronic inflammation causes the overproduction of free radical species and leads to oxidative stress, impairing the neuronal membrane [14, 15]. It is predisposed to oxidative stress due to higher ROS levels concomitant with limited counterregulatory measures. The various sections of our theme are narrow, we aim to shed light and expand the horizon on the current understanding of the relationship between APOE, gut microbiome, and oxidative damage in AD

Data sources and search terms
Selection criteria
Mitochondrial dysfunction and oxidative stress
Apolipoprotein E
Apolipoprotein E and oxidative stress
The gut microbiome
The gut microbiome and Apolipoprotein E
The gut microbiome and neurodegeneration
The gut microbiome and oxidative stress
Prospective interventional agents
Findings
Aim
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