Affiliations: [a] Programa de Pós-Graduação em Neurociências, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil | [b] Departamento de Bioquímica, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil
Correspondence:
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Corresponding author: Carlos-Alberto Gonçalves, Departamento de Bioquímica, ICBS, Universidade Federal do Rio Grande do Sul, Ramiro Barcelos, 2600-Anexo, 90035-003, Porto Alegre, RS, Brazil. E-mail: [email protected].
Abstract: Although the exact cause of Alzheimer's disease remains elusive, many possible risk factors and pathological alterations have been used in the elaboration of in vitro and in vivo models of this disease in rodents, including intracerebral infusion of streptozotocin (STZ). Using this model, we evaluated spatial cognitive deficit and neurochemical hippocampal alterations, particularly astroglial protein markers such as glial fibrillary acidic protein (GFAP) and S100B, glutathione content, nitric oxide production, and cerebrospinal fluid (CSF) S100B. In addition, prevention of these alterations by aminoguanidine administration was evaluated. Results confirm a spatial cognitive deficit and nitrative stress in this dementia model as well as specific astroglial alterations, particularly S100B accumulation in the hippocampus and decreased CSF S100B. The hippocampal astroglial activation occurred independently of the significant alteration in GFAP content. Moreover, all these alterations were completely prevented by aminoguanidine administration, confirming the neuroprotective potential of this compound, but suggesting that nitrative stress and/or glycation may be underlying these alterations. These findings contribute to the understanding of diseases accompanied by cognitive deficits and the STZ-model of dementia.
