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Curr Alzheimer Res. 2019;16(6):473-482. doi: 10.2174/1567205016666190503145207.

Inhibition of microRNA-155 Alleviates Cognitive Impairment in Alzheimer's Disease and Involvement of Neuroinflammation.

Author information

1
Center of Physical Examination, The First Hospital of Jilin University Changchun, Jilin 130021, China.
2
Department of Pediatric Gastroenterology, The First Hospital of Jilin University Changchun, Jilin 130021, China.
3
Department of Gerontology, The First Hospital of Jilin University Changchun, Jilin 130021, China.
4
Department of Thoracic Surgery The First Hospital of Jilin University Changchun, Jilin 130021, China.
5
Department of Cardiology, The First Hospital (Eastern Division) of Jilin University, Changchun, Jilin 130031, China.

Abstract

BACKGROUND:

Neuroinflammation has important effects on cognitive functions in the pathophysiological process of Alzheimer's Disease (AD). In the current report, we determined the effects of microRNA-155 (miR-155) on the levels of IL-1β, IL-6 and TNF-α, and their respective receptors in the hippocampus using a rat model of AD.

METHODS:

Real-time RT-PCR, ELISA and western blot analysis were used to examine the miR-155, PICs and PIC receptors. The Morris water maze and spatial working memory tests were used to assess cognitive functions.

RESULTS:

miR-155 was increased in the hippocampus of AD rats, accompanied by amplification of IL-1β, IL-6 and TNF-α. Intracerebroventricular infusion of miR-155 inhibitor, but not its scramble attenuated the increases of IL-1β, IL-6 and TNF-α and upregulation of their receptors. MiR-155 inhibitor also attenuated upregulation of apoptotic Caspase-3 in the hippocampus of AD rats. Notably, inhibition of miR- 155 or PIC receptors largely recovered the impaired learning performance in AD rat.

CONCLUSION:

We showed the critical role of miR-155 in regulating the memory impairment in AD rats likely via engagement of neuroinflammatory mechanisms, suggesting that miR-155 and its signaling molecules may present prospects in preventing and/or improving the development of the impaired cognitive functions in AD.

KEYWORDS:

Alzheimer's disease; Caspase-3; hippocampus; miroRNA-155; neuroinflammation; pro-inflammatory cytokines.

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