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Neurobiol Aging ; 36(11): 2984-2994, 2015 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-26264859

RESUMO

Although metabolic syndrome was suggested to be a risk factor for Alzheimer's disease (AD), the role of metabolic stress in the initiation of AD pathology remains unclear. In this study, metabolic stress was induced by a high-fat diet and low-dose injection of streptozotocin (HFSTZ) before the appearance of senile plaques in APP/PS1 transgenic mice. We found that, HFSTZ treatment exacerbated amyloid beta burden and astrocyte activation in the vicinity of plaques. Moreover, we observed an upregulation of astrocytic S100B expression in the brain parenchyma of HFSTZ-treated APP/PS1 mice concurrent with increased interleukin-6 expression in cerebral microvascular cells. To determine the impact of HFSTZ treatment on brain function, we performed [(18)F]fludeoxyglucose-positron emission tomography and analyzed nesting behavior. HFSTZ treatment impaired nest construction and cerebral glucose metabolism in several brain regions of APP/PS1 mice during the early stage of AD. These results suggest that HFSTZ-induced peripheral metabolic stress may contribute to vascular inflammation and astrocyte reactivity in the parenchyma and may impair activity of daily living skill and cerebral glucose metabolism in APP/PS1 mice.


Assuntos
Astrócitos/metabolismo , Astrócitos/patologia , Encéfalo/metabolismo , Transtornos Cognitivos/etiologia , Glucose/metabolismo , Estresse Fisiológico/fisiologia , Doença de Alzheimer/etiologia , Peptídeos beta-Amiloides/metabolismo , Animais , Encéfalo/irrigação sanguínea , Proteína Glial Fibrilar Ácida/metabolismo , Interleucina-6/metabolismo , Masculino , Síndrome Metabólica/etiologia , Camundongos Transgênicos , Microvasos/metabolismo , Obesidade/etiologia , Placa Amiloide/metabolismo , Placa Amiloide/patologia , Subunidade beta da Proteína Ligante de Cálcio S100/metabolismo , Estreptozocina
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