期刊
NEUROBIOLOGY OF AGING
卷 35, 期 7, 页码 1744-1754出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.neurobiolaging.2014.01.012
关键词
MCAO; Inflammation; Aging; Depression
资金
- European Union [LSHB-CT-2006-018936]
- research program of the Jena Centre for Systems Biology of Ageing-Jenage [BMBF 0315581]
Increased age is a major risk factor for stroke incidence and post-ischemic mortality. To develop age-adjusted therapeutic interventions, a clear understanding of the complexity of age-related post-ischemic mechanisms is essential. Transient occlusion of the middle cerebral arteryda model that closely resembles human strok-was used to induce cerebral infarction in mice of 4 different ages (2, 9, 15, 24 months). By using Illumina cDNA microarrays and quantitative PCR we detected a distinct age-dependent response to stroke involving 350 differentially expressed genes. Our analyses also identified 327 differentially expressed genes that responded to stroke in an age-independent manner. These genes are involved in different aspects of the inflammatory and immune response, oxidative stress, cell cycle activation and/or DNA repair, apoptosis, cytoskeleton reorganization and/or astrogliosis, synaptic plasticity and/or neurotransmission, and depressive disorders and/or dopamine-, serotonin-, GABA-signaling. In agreement with our earlier work, aged brains displayed an attenuated inflammatory and immune response (Sieber et al., 2011) and a reduced impairment of post-stroke synaptic plasticity. Our data also revealed a distinct age-related susceptibility for post-ischemic depression, the most common neuropsychiatric consequence of stroke, which has a major influence on functional outcome. (C) 2014 Elsevier Inc. All rights reserved.
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