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Int. J. Mol. Sci. 2014, 15(12), 22092-22108;

TGF-β1 Protection against Aβ1–42-Induced Neuroinflammation and Neurodegeneration in Rats

School of Biological & Basic Medical Sciences, Soochow University, 199 Renai Road, Suzhou 215123, China
Department of Physiology, School of Medicine, Nantong University, 19 Qixiu Road, Nantong 226001, China
Co-innovation Center of Neuroregeneration, Nantong University, 19 Qixiu Road, Nantong 226001, China
Authors to whom correspondence should be addressed.
Received: 15 August 2014 / Revised: 31 October 2014 / Accepted: 14 November 2014 / Published: 1 December 2014
(This article belongs to the Special Issue Neuroprotective Strategies 2014)
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Transforming growth factor (TGF)-β1, a cytokine that can be expressed in the brain, is a key regulator of the brain’s responses to injury and inflammation. Alzheimer’s disease (AD), the most common neurodegenerative disorder, involves inflammatory processes in the brain in addition to the hallmarks, amyloid-β (Aβ) plaques and neurofibrillary tangles. Recently, we have shown that T-helper (Th) 17 cells, a subpopulation of CD4+ T-cells with high proinflammation, also participate in the brain inflammatory process of AD. However, it is poorly known whether TGF-β1 ameliorates the lymphocyte-mediated neuroinflammation and, thereby, alleviates neurodegeneration in AD. Herein, we administered TGF-β1 via the intracerebroventricle (ICV) in AD model rats, by Aβ1–42 injection in both sides of the hippocampus, to show the neuroprotection of TGF-β1. The TGF-β1 administration after the Aβ1–42 injection ameliorated cognitive deficit and neuronal loss and apoptosis, reduced amyloid precursor protein (APP) expression, elevated protein phosphatase (PP)2A expression, attenuated glial activation and alleviated the imbalance of the pro-inflammatory/anti-inflammatory responses of T-lymphocytes, compared to the Aβ1–42 injection alone. These findings demonstrate that TGF-β1 provides protection against AD neurodegeneration and suggest that the TGF-β1 neuroprotection is implemented by the alleviation of glial and T-cell-mediated neuroinflammation. View Full-Text
Keywords: TGF-β1; Alzheimer’s disease; Aβ1–42; T-lymphocytes; microglia TGF-β1; Alzheimer’s disease; 1–42; T-lymphocytes; microglia

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Shen, W.-X.; Chen, J.-H.; Lu, J.-H.; Peng, Y.-P.; Qiu, Y.-H. TGF-β1 Protection against Aβ1–42-Induced Neuroinflammation and Neurodegeneration in Rats. Int. J. Mol. Sci. 2014, 15, 22092-22108.

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