【摘 要】
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Objective One of the neuropathological features of Alzheimers disease (AD) is high density of senile plaques, mainly composed of amyloid β protein (Aβ).It has been found that type 2 diabetes mellitus
【机 构】
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Department of Physiology, Shanxi Medical University, Taiyuan 030001, China
【出 处】
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中国神经科学学会第九届全国学术会议暨第五届会员代表大会
论文部分内容阅读
Objective One of the neuropathological features of Alzheimers disease (AD) is high density of senile plaques, mainly composed of amyloid β protein (Aβ).It has been found that type 2 diabetes mellitus (T2DM) is a risk factor for developing AD.One promising treatment for AD is using glucagon-like peptide-1 (GLP-1), a modulator used in T2DM therapy.To characterize the neuroprotective role and possible mechanism of GLP-1 in the brain, we investigated the effects of Val8-GLP-1 (7-36), a GLP-1 analogue with greater biological activity, on the Aβ1-40-induced neurotoxicity.Methods We investigated: (1) the effects of Intracerebraventricular (i.c.v.) injection of Val8-GLP-1(7-36) on the Aβ1-40-induced impairment of spatial learning and memory of rats in Morris water maze test; (2) the effects of i.c.v.injection of Val8-GLP-1(7-36) on the Aβ1-40-induced impairment of in vivo late phase of long-term potentiation (L-LTP) in rat hippocampal CA1 region; (3) the effects of ValLGLP-1(7-36) on the Aβ1-40-induced changes in miniature postsynaptic currents (mEPSCs and mIPSCs) in rat hippocampal CA1 pyramidal neurons; (4) the effects of pretreatment with Val8-GLP-1 (7-36) on Aβ1-40-induced elevation of [Ca2+]i in cultured primary rat cortical neurons.Results (1) Pretreatment with Val8-GLP-1(7-36) (0.05 pmol, 0.5 pmol or 5 pmol) effectively reversed Aβ1-40 (5 nmol)-induced impairment of cognitive function in a dose dependent manner.(2) Pretreatment with Val8-GLP-1(7-36) effectively reversed Aβ1-40 (5 nmol)-induced suppression of L-LTP in a dose-dependent manner.(3) Pretreatment with Val8-GLP-1(7-36) (10 nM) prevented the Aβ1-40 (100 nM)-induced decrease of frequency of mEPSCs and mIPSCs.(4) Pretreatment with Val8-GLP-1(7-36) (10 nM, 100 nM or 1000 nM) effectively protected against Aβ1-40 (10 μM)-induced elevation of [Ca2+]i in a dose-dependent manner.Conclusion GLP-1 plays an important positive role in attenuating Aβ-induced deficits and stable GLP-1 analogues such as Val8-GLP-1 (7-36) could be an effective promising strategy for AD patients, particularly when associate with T2DM.
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