Mitochondrial defects and oxidative stress in Alzheimer disease and Parkinson disease

Abstract

Alzheimer disease (AD) and Parkinson disease (PD) are the two most common age-related neurodegenerative diseases characterized by prominent neurodegeneration in selective neural systems. Although a small fraction of AD and PD cases exhibit evidence of heritability, among which many genes have been identified, the majority are sporadic without known causes. Molecular mechanisms underlying neurodegeneration and pathogenesis of these diseases remain elusive. Convincing evidence demonstrates oxidative stress as a prominent feature in AD and PD and links oxidative stress to the development of neuronal death and neural dysfunction, which suggests a key pathogenic role for oxidative stress in both AD and PD. Notably, mitochondrial dysfunction is also a prominent feature in these diseases, which is likely to be of critical importance in the genesis and amplification of reactive oxygen species and the pathophysiology of these diseases. In this review, we focus on changes in mitochondrial DNA and mitochondrial dynamics, two aspects critical to the maintenance of mitochondrial homeostasis and function, in relationship with oxidative stress in the pathogenesis of AD and PD.

Nutritional contributions to dementia prevention: main issues on antioxidant micronutrients

“…In the absence of an adequate antioxidant defense system, ROS and RNS damage to body lipids, nucleic acids and proteins has been consistently shown to be associated with the presence of AD-related alterations and symptoms as well as to disease severity. By-products of oxidative stress and redox unbalanced regulation as well as antioxidant depletion independent of diet have been repeatedly observed in plasma and tissues of patients with cognitive impairment even long prior to overt dementia manifestation (Praticó et al 2002;Rinaldi et al 2003) suggesting chronological primacy of oxidative stress in AD (Smith et al 2005;Yan et al 2013). The involvement of oxidative stress at different levels in AD in neuronal mitochondria is particularly deleterious due to their susceptibility to oxidative damage.…”

Synthesis and evaluation of frentizole-based indolyl thiourea analogues as MAO/ABAD inhibitors for Alzheimer’s disease treatment

“…aldehydes or hydrogen peroxide), 15 which consequently promote already ongoing oxidative stress in AD. 16 Taken together, targeting both MAO-A and MAO-B could potentially contribute to therapeutic effects in AD treatment.…”

Physicochemical properties and in-vitro antioxidant capacity of Semen Astragali Complanati wine

“…Reactive oxygen species play a dual role in biological systems: a positive role at a lower or moderate concentrations during normal physiological and biochemical processes and a negative role in excess, causing oxidative stress and resulting in a number of diseases (Valko et al, 2007), such as cardiovascular, cancer (Gaetano, Francesco, & Gianluigi, 2013), immune dysfunctions and neurodegenerative disorders (Huang, Ou, & Prior, 2005;Yan, Wang, & Zhu, 2013). Recently, an epidemiological survey demonstrated the efficiency of intake antioxidants (synthetic or natural) in preventing or suppressing free-radical-related diseases (Pérez-Jiménez & Saura-Calixto, 2015).…”