Journal
OXIDATIVE MEDICINE AND CELLULAR LONGEVITY
Volume 2018, Issue -, Pages -Publisher
HINDAWI LTD
DOI: 10.1155/2018/1358057
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Funding
- VIEP-BUAP [DIFA-NAT17-I, MAMG-NAT17-I, TRMS-NAT17-I]
- PRODEP [511-6/17-8017, BUAP-PTC-550, BUAP-PTC-577]
- PAPIIT-UNAM [IN214117]
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An important worldwide health problem as the result of current lifestyle is metabolic syndrome (MS). It has been shown that MS induced by a high-calorie diet (HCD) in rats produces cognitive deterioration in the novel object recognition test (NORt) and decreases synaptic connections and dendritic order in the hippocampus and temporal cortex. However, it is unknown whether MS induced by an HCD participates in the cognitive process observed with the injection of A beta(1-42) into the hippocampus of rats as a model of Alzheimer disease (AD). The induction of MS in rats produces a deterioration in NORt; however, rats with MS injected with A beta(1-42) show a major deterioration in the cognitive process. This event could be explained by the increment in the oxidative stress in both cases studied (MS and A beta(1-42)): together, the hippocampus and temporal cortex produce an enhancer effect. In the same way, we observed an increment in interleukin-1 beta, TNF-alpha, and GFAP, indicative of exacerbated inflammatory processes by the combination of MS and A beta(1-42). We can conclude that MS might play a key role in the apparition and development of cognitive disorders, including AD. We propose that metabolic theory is important to explain the apparition of cognitive diseases.
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