胆碱能的
神经毒性
神经科学
神经保护
突触素
胆碱能神经元
药理学
医学
生物
毒性
内科学
免疫学
免疫组织化学
作者
Chiara Burgaletto,Giulia Di Benedetto,Antonio Munafò,Renato Bernardini,Giuseppina Cantarella
标识
DOI:10.2174/1567205018666210608093658
摘要
Alzheimer's disease (AD) is the most common form of neurodegenerative disorder characterized by cognitive impairment, which represents an urgent public health concern. Given the worldwide impact of AD, there is a compelling need for effective therapies to slow down or halt this disorder.Choline alphoscerate (α-GPC) represents a potentially effective cholinergic neurotransmission enhancing agent with an interesting clinical profile in cognitive dysfunctions improvement, although only scanty data are available about the mechanisms underlying such beneficial effects.The SH-SY5Y neuronal cell line, differentiated for 1 week with 10 μm of all-trans-retinoic acid (RA), to achieve a switch towards a cholinergic phenotype, was used as an in vitro model of AD. SH-SY5Y cells were pre-treated for 1h with α-GPC (100nM) and treated for 72 h with Aβ25-35 (10μM).α-GPC was able to antagonize Aβ25-35 mediated neurotoxicity and attenuate the Aβ-induced phosphorylation of the Tau protein. Moreover, α-GPC exerted its beneficial effects by employing the NGF/TrkA system, knocked down in AD and, consequently, by sustaining the expression level of synaptic vesicle proteins, such as synaptophysin.Taken together, our data suggest that α-GPC can have a role in neuroprotection in the course of toxic challenges with Aβ. Thus, a deeper understanding of the mechanism underlying its beneficial effect, could provide new insights into potential future pharmacological applications of its functional cholinergic enhancement, with the aim to mitigate AD and could represent the basis for innovative therapy.
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