Format

Send to

Choose Destination
Synapse. 2017 Jun 26. doi: 10.1002/syn.21990. [Epub ahead of print]

Alzheimer's disease and metabolic syndrome: A link from oxidative stress and inflammation to neurodegeneration.

Author information

1
Departamento de Bioquímica, Facultad de Medicina, Universidad Nacional Autónoma de México, Ciudad de México, Mexico.
2
Facultad de Ciencias Químicas, Benemérita Universidad Autónoma de Puebla, Puebla, Pue, Mexico.
3
Departamento de Bioquímica, Instituto Nacional de Enfermedades Respiratorias-INER, Ciudad de México, Mexico.
4
Instituto de Fisiología, Benemérita Universidad Autónoma de Puebla, Puebla, Pue, Mexico.

Abstract

Alzheimer's disease (AD) is the most common cause of dementia and one of the most important causes of morbidity and mortality among the aging population. AD diagnosis is made post-mortem, and the two pathologic hallmarks, particularly evident in the end stages of the illness, are amyloid plaques and neurofibrillary tangles. Currently, there is no curative treatment for AD. Additionally, there is a strong relation between oxidative stress, metabolic syndrome, and AD. The high levels of circulating lipids and glucose imbalances amplify lipid peroxidation that gradually diminishes the antioxidant systems, causing high levels of oxidative metabolism that affects cell structure, leading to neuronal damage. Accumulating evidence suggests that AD is closely related to a dysfunction of both insulin signaling and glucose metabolism in the brain, leading to an insulin-resistant brain state. Four drugs are currently used for this pathology: Three FDA-approved cholinesterase inhibitors and one NMDA receptor antagonist. However, wide varieties of antioxidants are promissory to delay or prevent the symptoms of AD and may help in treating the disease. Therefore, therapeutic efforts to achieve attenuation of oxidative stress could be beneficial in AD treatment, attenuating Aβ-induced neurotoxicity and improve neurological outcomes in AD. The term inflammaging characterizes a widely accepted paradigm that aging is accompanied by a low-grade chronic up-regulation of certain pro-inflammatory responses in the absence of overt infection, and is a highly significant risk factor for both morbidity and mortality in the elderly.

KEYWORDS:

Alzheimer; amyloid-β; diabetes; free radicals; glucose; metabolic syndrome; neurodegeneration; oxidative stress; tau

PMID:
28650104
DOI:
10.1002/syn.21990

Supplemental Content

Loading ...
Support Center