Neuronal failure in Alzheimer’s disease: a view through the oxidative stress looking-glass

Abstract

There is considerable debate and controversy surrounding the cause(s) of Alzheimer disease (AD). To date, several theories have gained notoriety, however there has yet to be any one that garners universal acceptance. In this review, we provide evidence for the oxidative stress-induced AD cascade that posits aged mitochondria as the critical origin of neurodegeneration in AD.

Air pollution, a rising environmental risk factor for cognition, neuroinflammation and neurodegeneration: The clinical impact on children and beyond

“…If cellular defense mechanisms try to intervene but fail, as strongly suggested by several authors [86], and gene studies point towards the strong association with networks characterized by the very same common denominators i.e., oxidative stress, seen in common diseases that are causing high morbility and mortality (cancer, diabetes, renal diseases, and cardiovascular diseases), then why not pursue the notion that gene changes and the pathology in urban children is indicative of an active host response or environmental adaptation as suggested by Castellani and Perry [56].…”

Mexico City normal weight children exposed to high concentrations of ambient PM2.5 show high blood leptin and endothelin-1, vitamin D deficiency, and food reward hormone dysregulation versus low pollution controls. Relevance for obesity and Alzheimer disease

“…If so, since leptin plays a key role in the developing brain (Steppan and Swick, 1999;Stieg et al, 2015;Farr et al, 2014;Bouret, 2010;Johnston et al, 2014;Pérez-González et al, 2011;Busch et al, 2011;Folch et al, 2012;Zhang et al, 2013;Mancini et al, 2014;Davis et al, 2014) are the high leptin concentrations in serum associated with high CSF leptin and low leptin receptors mRNA in target areas like hippocampus as in Alzheimer's patients? (Bonda et al, 2014a(Bonda et al, , 2014b. If indeed, aberrant leptin signaling is present in urban children as in patients with neuroinflammatory entities, i.e., AIDS and Alzheimer's disease (Bonda et al, 2014a(Bonda et al, , 2014bHuang et al, 2007;Johnston et al, 2014) will children's brain development be compromised?…”

“…(Bonda et al, 2014a(Bonda et al, , 2014b. If indeed, aberrant leptin signaling is present in urban children as in patients with neuroinflammatory entities, i.e., AIDS and Alzheimer's disease (Bonda et al, 2014a(Bonda et al, , 2014bHuang et al, 2007;Johnston et al, 2014) will children's brain development be compromised? Given that leptin dysregulation is a key finding in AD (Bonda et al, 2014a(Bonda et al, , 2014b …”

Inflammatory Cytokines and Alzheimer’s Disease: A Review from the Perspective of Genetic Polymorphisms

“…However, the exact mechanisms by which AD occurs and develops remain ill-defined, and effective methods to cure the disease or halt the associated cognitive decline remain undiscovered. Nevertheless, neuroinflammation and oxidative stress have received increasing attention as accumulating evidence suggests their involvement in its development [2,3]. Activation of microglia, the brain-specific macrophages, has been reported in both AD patients and animal models [4], accompanied by an activated complement system [5] and increased levels of chemokines and cytokines [6,7].…”