title: Oxidative stress and metabolic syndrome: cause or consequence of Alzheimer's disease?
abstract: Alzheimer's disease (AD) is a major neurodegenerative disease affecting the elderly. Clinically, it is characterized by a progressive loss of memory and cognitive function. Neuropathologically, it is characterized by the presence of extracellular β-amyloid (Aβ) deposited as neuritic plaques (NP) and neurofibrillary tangles (NFT) made of abnormal and hyperphosphorylated tau protein. These lesions are capable of generating the neuronal damage that leads to cell death and cognitive failure through the generation of reactive oxygen species (ROS). Evidence indicates the critical role of Aβ metabolism in prompting the oxidative stress observed in AD patients. However, it has also been proposed that oxidative damage precedes the onset of clinical and pathological AD symptoms, including amyloid-β deposition, neurofibrillary tangle formation, vascular malfunction, metabolic syndrome, and cognitive decline. This paper provides a brief description of the three main proteins associated with the development of the disease (Aβ, tau, and ApoE) and describes their role in the generation of oxidative stress. Finally, we describe the mitochondrial alterations that are generated by Aβ and examine the relationship of vascular damage which is a potential prognostic tool of metabolic syndrome. In addition, new therapeutic approaches targeting ROS sources and metabolic support were reported.
authors.affiliation: Facultad de Ciencias Químicas, Universidad Autónoma de Coahuila, Boulevard V. Carranza S/N, Colonia República Oriente, Saltillo, COAH, Mexico.
authors.forename: Diana
authors.initials: D
authors.lastname: Luque-Contreras
authors.affiliation: Laboratorio de Nutrición Experimental, Instituto Nacional de Pediatría, Insurgentes Sur 3700 letra C, Coyoacán, 04530 Mexico City, Mexico.
authors.forename: Karla
authors.initials: K
authors.lastname: Carvajal
authors.affiliation: Departamento de Fisiología Biofísica y Neurociencias, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional, Instituto Politécnico Nacional, 2508, 07360 Mexico City, Mexico.
authors.forename: Danira
authors.identifier: 0000-0001-5156-6969
authors.initials: D
authors.lastname: Toral-Rios
authors.affiliation: Universidad Nacional Autónoma de México, Avenida Insurgentes Sur 3000, Coyoacán, 04510 Mexico City, Mexico.
authors.forename: Diana
authors.initials: D
authors.lastname: Franco-Bocanegra
authors.affiliation: Laboratorio Experimental de Enfermedades Neurodegenerativas, Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Suárez, Insurgentes Sur 3877, 14269 Mexico City, Mexico.
authors.forename: Victoria
authors.initials: V
authors.lastname: Campos-Peña
mesh_terms: D000544:Alzheimer Disease / Q000150:complications* / Q000473:pathology*; D004730:Endothelium, Vascular / Q000473:pathology; D006801:Humans; D024821:Metabolic Syndrome / Q000150:complications* / Q000473:pathology*; D008928:Mitochondria / Q000378:metabolism / Q000473:pathology; D018384:Oxidative Stress; D012084:Renin-Angiotensin System