2012
DOI: 10.1016/j.bbr.2011.09.035
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Neuroglial alterations in rats submitted to the okadaic acid-induced model of dementia

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Cited by 54 publications
(43 citation statements)
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“…Since astrocytes are essential for maintaining neuronal activity, disruption of their function may contribute to neuronal injury in manganism (Gonzalez et al, 2008). Of particular importance, astrocytic activation has been associated with oxidative stress (Andersen, 2004) and decreased GSH levels (Enongene et al, 2000;Costa et al, 2012), consistent with our results.…”
Section: Discussionsupporting
confidence: 88%
“…Since astrocytes are essential for maintaining neuronal activity, disruption of their function may contribute to neuronal injury in manganism (Gonzalez et al, 2008). Of particular importance, astrocytic activation has been associated with oxidative stress (Andersen, 2004) and decreased GSH levels (Enongene et al, 2000;Costa et al, 2012), consistent with our results.…”
Section: Discussionsupporting
confidence: 88%
“…OKA significantly enhanced in GFAP mRNA level suggesting the role of the astrocyte activation in OKA induced cognitive deficits. These finding are accordance to Costa et al (2012). In previous study also, we found that Lipopolysaccharide (LPS) has significantly up regulated GFAP protein expression in astroglial cells mimicking the reactive gliosis during in vivo patho-physiological conditions of neurodegenerative disease like Alzheimer's disease (Niranjan et al, 2010).…”
Section: Discussionsupporting
confidence: 89%
“…Together with apoptosis induction, cytoskeleton disruption, or cell cycle alterations, OA was also shown to induce oxidative stress in a number of in vitro and in vivo studies [70,71,72], and to affect different catabolic and anabolic pathways—including glycolysis, lipolysis, and gluconeogenesis—in several cell types [15,53]. Besides, the expression of different metabolism-related genes was found to be altered after OA exposure [73].…”
Section: Oa Beyond Its Role As Dsp Inductormentioning
confidence: 99%
“…Tau protein is responsible, among others, for microtubule stabilization, maintenance of long-term potentiation, learning and memory, and its abnormally phosphorylated form is considered one of the pathological hallmarks of Alzheimer’s disease [88]. Accordingly, OA is currently employed as a useful tool to screen potential drugs for prevention and treatment of Alzheimer’s disease and other dementia forms [70,83,89,90]. …”
Section: Oa Beyond Its Role As Dsp Inductormentioning
confidence: 99%