Cunliffe Grace, Lim Yi Tang, Chae Woori, Jung Sangyong
Institute of Molecular and Cell Biology (IMCB), Agency for Science, Technology and Research (A*STAR), Singapore 138667, Singapore.
Division of Neuroscience and Experimental Psychology, School of Biological Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester M13 9PL, UK.
Biomedicines. 2022 Nov 28;10(12):3064. doi: 10.3390/biomedicines10123064.
Alzheimer's disease (AD) is a neurodegenerative disorder, comprising 70% of dementia diagnoses worldwide and affecting 1 in 9 people over the age of 65. However, the majority of its treatments, which predominantly target the cholinergic system, remain insufficient at reversing pathology and act simply to slow the inevitable progression of the disease. The most recent neurotransmitter-targeting drug for AD was approved in 2003, strongly suggesting that targeting neurotransmitter systems alone is unlikely to be sufficient, and that research into alternate treatment avenues is urgently required. Neuromodulators are substances released by neurons which influence neurotransmitter release and signal transmission across synapses. Neuromodulators including neuropeptides, hormones, neurotrophins, ATP and metal ions display altered function in AD, which underlies aberrant neuronal activity and pathology. However, research into how the manipulation of neuromodulators may be useful in the treatment of AD is relatively understudied. Combining neuromodulator targeting with more novel methods of drug delivery, such as the use of multi-targeted directed ligands, combinatorial drugs and encapsulated nanoparticle delivery systems, may help to overcome limitations of conventional treatments. These include difficulty crossing the blood-brain-barrier and the exertion of effects on a single target only. This review aims to highlight the ways in which neuromodulator functions are altered in AD and investigate how future therapies targeting such substances, which act upstream to classical neurotransmitter systems, may be of potential therapeutic benefit in the sustained search for more effective treatments.
阿尔茨海默病(AD)是一种神经退行性疾病,占全球痴呆症诊断病例的70%,在65岁以上人群中,每9人就有1人受其影响。然而,其大多数主要针对胆碱能系统的治疗方法,在逆转病理方面仍然效果不佳,只是简单地减缓疾病不可避免的进展。最近一种用于治疗AD的靶向神经递质的药物于2003年获批,这有力地表明仅靶向神经递质系统不太可能足够,迫切需要研究其他治疗途径。神经调质是由神经元释放的物质,可影响神经递质的释放和突触间的信号传递。包括神经肽、激素、神经营养因子、ATP和金属离子在内的神经调质在AD中功能发生改变,这是异常神经元活动和病理的基础。然而,关于如何操纵神经调质可能对AD治疗有用的研究相对较少。将靶向神经调质与更新颖的药物递送方法相结合,如使用多靶点定向配体、组合药物和纳米颗粒封装递送系统,可能有助于克服传统治疗的局限性。这些局限性包括难以穿过血脑屏障以及仅对单一靶点产生作用。本综述旨在强调AD中神经调质功能改变的方式,并研究针对这些作用于经典神经递质系统上游物质的未来疗法,在持续寻找更有效治疗方法的过程中可能具有的潜在治疗益处。