ArticleMetabolic brain disease2015
Characterization of prefrontal cortex microstructure and antioxidant status in a rat model of neurodegeneration induced by aluminium chloride and multiple low-dose streptozotocin.
Article in Metabolic brain disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 9 citations in OpenAlex.
- Neuroprotective, antidiabetic and antioxidant effect of Hedera nepalensis and lupeol against STZ + AlClDaru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2018Article
- Altered temporal lobe white matter lipid ion profiles in an experimental model of sporadic Alzheimer's disease.Molecular and cellular neurosciences · 2017Article
- Sweet old memories: a review of the experimental models of the association between diabetes, senility and dementia.Metabolic brain disease · 2016Review
- Targeting Alzheimer's Disease Neuro-Metabolic Dysfunction with a Small Molecule Nuclear Receptor Agonist (T3D-959) Reverses Disease Pathologies.Journal of Alzheimer's disease & Parkinsonism · 2016Article
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetes mellitus (DM) is a risk factor for Alzheimer's disease (AD), and several individuals with AD are diabetic. Most non-transgenic animal models of AD make use of oral treatment with aluminium chloride (AlCl(3)) to induce brain lesions pathognomonic of the disease. Moreover, streptozotocin (STZ) can induce pathological features of either AD or DM depending on the mode of treatment. In the present study, we characterised prefrontal microanatomy and antioxidant defence system in a rat model of AD confounded by DM, with the objective of assessing the suitability of this model in the study of sporadic AD with DM co-morbidity. Adult Wistar rats were randomly assigned to receive either intraperitoneal STZ (30 mg/kg/day for 3 days; to induce DM), oral AlCl(3) (500 mg/kg/day for 4 weeks; to induce some brain lesions characteristic of AD); or both STZ and AlCl(3) (to induce AD with DM co-morbidity). Untreated rats served as controls. During treatment, blood glucose levels and body weights were evaluated repeatedly in all rats. At euthanasia, prefrontal cortex was homogenized in phosphate buffer solution and the supernatants assayed for some antioxidant enzymes (catalase, CAT; superoxide dismutase, SOD; and reduced glutathione, GSH). Moreover, following perfusion-fixation of the brain, frontal lobes were processed by the haematoxylin and eosin (H&E) or Congo red technique. Our findings showed that in rats co-administered AlCl(3) and STZ (AD + DM rats), prefrontal levels of GSH reduced significantly (p < 0.05), while reductions in SOD and CAT were not significant (p > 0.05) compared with the controls. Moreover, in this model of AD with DM co-morbidity, extensive neuronal cell loss was observed in the prefrontal cortex, but Congophilic deposits were not present. The neurodegenerative lesions and antioxidant deficits characteristic of this AlCl(3) + STZ (AD + DM) rat model were more pronounced than similar lesions associated with mono-treatment with either STZ (DM) or AlCl(3) (AD) alone; and this makes the AlCl(3) + STZ model a suitable option for the study of neurodegenerative diseases (such as AD) with DM co-morbidity.
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