期刊
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM
卷 40, 期 2, 页码 446-455出版社
SAGE PUBLICATIONS INC
DOI: 10.1177/0271678X19825785
关键词
Ischemic stroke; memory dysfunction; bone fracture; stroke recovery; neuroinflammation
资金
- NHLBI NIH HHS [R01 HL122774] Funding Source: Medline
- NINDS NIH HHS [R21 NS070153, R21 NS083788] Funding Source: Medline
Cognitive impairment occurs in stroke and hip fracture patients. In mice, bone fracture (BF) exacerbates stroke-related neuronal damage and sensorimotor dysfunction. We hypothesize that BF exacerbates post-stroke cognitive impairment. Adult mice were randomly assigned into BF, stroke, BF+stroke (BF 6 h before stroke), and control (sham operated) groups. Memory function was evaluated weekly for eight weeks by Y maze test and at eight weeks post-surgeries by novel object recognition (NOR) test. The neuronal damage and inflammation in hippocampus were analyzed three days and eight weeks after the surgeries. In Y maze test, BF+stroke mice started making fewer alternations than controls two weeks after the surgeries. Significant difference between BF+stroke and stroke groups started at five weeks post-injury and continued to the end of the experiment. In NOR test, BF+stroke group spent less time on novel objective than that of other groups. Cx3cr1(+) cells and CD68(+) cells accumulated in the stratum lacunosum moleculare (SLM) on the ipsilateral side of stroke injury in stroke and BF+stroke mice. BF+stroke mice had a higher ratio of ipsilateral/contralateral Cx3cr1(+) cell-density than that of stroke mice. Therefore, BF shortly before stroke exacerbates hippocampal inflammation and causes long-lasting memory dysfunction.
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