Metabolic Syndrome Exacerbates the Recognition Memory Impairment and Oxidative-Inflammatory Response in Rats with an Intrahippocampal Injection of Amyloid Beta 1–42

<div>The injection of A<i>β</i><sub>1–42</sub> into the hippocampus increases the concentration of proinflammatory cytokines in HCD-fed rats. (a) IL-1<i>β</i> in the temporal cortex. (b) IL-1<i>β</i> in the hippocampus. (c) TNF-<i>α</i> in the temporal cortex. (d) TNF-<i>α</i> in the hippocampus. Metabolic syndrome induced by HCD and injection with A<i>β</i><sub>1–42</sub> increase the concentration of IL-1<i>β</i> and TNF-<i>α</i>, in the TCx and hippocampus (a–d). The mean of data ± SE is plotted. 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Oxidative Medicine and Cellular Longevity

fig5

Figure 5

Figure 5: Metabolic Syndrome Exacerbates the Recognition Memory Impairment and Oxidative-Inflammatory Response in Rats with an Intrahippocampal Injection of Amyloid Beta 1–42 

Figure 5 | Metabolic Syndrome Exacerbates the Recognition Memory Impairment and Oxidative-Inflammatory Response in Rats with an Intrahippocampal Injection of Amyloid Beta 1–42 