A review on mitochondrial restorative mechanism of antioxidants in Alzheimer’s disease and other neurological conditions

Abstract

Neurodegenerative diseases are intricate in nature because of the involvement of the multiple pathophysiological events including mitochondrial dysfunction, neuroinflammation and oxidative stress. Alzheimer’s disease (AD) is a neurodegenerative disease explained by extracellular amyloid β deposits, intracellular neurofibrillary tangles and mitochondrial dysfunction. Increasing evidence has indicated that mitochondrial dysfunction displays significant role in the pathophysiological processes of AD. Mitochondrial dysfunction involves alterations in mitochondrial respiratory enzyme complex activities, oxidative stress, opening of permeability transition pore, and enhanced apoptosis. Various bioenergetics and antioxidants have been tried or under different investigational phase against AD and other neurodegenerative disorders (Parkinson’s disease, Huntington’s disease, and Amyotrophic lateral sclerosis) because of their complex and multiple site of action. These mitochondrial-targeting bioenergetics and antioxidant compounds such as coenzyme Q10, idebenone, creatine, mitoQ, mitovitE, MitoTEMPOL, latrepirdine, methylene blue, triterpenoids, SS peptides, curcumin, Ginkgo biloba, and omega-3 polyunsaturated fatty acids with potential efficacy in AD have been identified. Present review is intent to discuss mitochondrial restorative mechanisms of these bioenergetics and antioxidants as a potential alternative drug strategy for effective management of AD.

Neurodegeneration and Alzheimer's disease (AD). What Can Proteomics Tell Us About the Alzheimer's Brain?

“…The idea that oxidative damage and mitochondrial dysfunction is central to AD pathology has garnered support throughout the years (123,124), and proteomic analyses that have been performed in the AD post mortem brain and Tg AD animal models support these findings. To obtain further insights into this process and to understand the order of AD pathological events, proteomics studies in Tg AD model mouse might be of great interest.…”

“…This hinders both the ubiquitin proteasome system and the lysosomal-autophagy process, resulting in the early loss of synaptic contacts. Targeting these processes may provide therapeutic interventions and future studies (124). However, this is easier said than done, as the affected pathways are highly complex and regulated.…”

Curcumin partly ameliorates irinotecan-induced diarrhea and synergistically promotes apoptosis in colorectal cancer through mediating oxidative stress

“…Curcumin could protect mitochondria by scavenging ROS, inhibiting mitochondrial swelling, increasing the activities of antioxidant enzymes, and ameliorating mitochondrial dysfunction ultimately by improving energy metabolism [36][37][38]. What's more, it has been reported that curcumin could relieve HIVrelated diarrhea by decreasing mucosal permeability through mucosal inflammatory pathways [19].…”

β-Amyloid Biomarker Detection for Alzheimer’s Disease

“…Current studies are taking into account the role that Ab oligomers have played in synaptic impairment and their relationship to brain functioning [3]. The Ab protein is made up of 39-42 amino acids, which are the main components of the plaques found in the AD brain.…”

“…The foremost pathophysiology of this disease is the accumulation of protein beta amyloid (Ab) in the extracellular space and neurofibrillary tangles containing the microtubule-associated tau protein in the intracellular space [1,3]. Current studies are taking into account the role that Ab oligomers have played in synaptic impairment and their relationship to brain functioning [3].…”