Aslan Feyza Sule, Akdag Mahmut Berat, Doganyigit Zuleyha, Okan Aslı, Shaikh Mohd Farooq, Akyuz Enes
School of Medicine, Marmara University, Istanbul, Türkiye.
Vocational School, Physiotherapy Program, Istanbul Atlas University, Istanbul, Türkiye.
J Neurosci Res. 2025 Apr;103(4):e70033. doi: 10.1002/jnr.70033.
Central nervous system (CNS) disorders, such as Alzheimer's disease (AD), Parkinson's disease (PD), multiple sclerosis (MS), and migraines, rank among the most prevalent and concerning conditions worldwide. Despite ongoing research, the pathophysiology of these disorders remains incompletely understood, primarily due to their complex etiology. Current pharmacological treatments mainly focus on alleviating symptoms rather than addressing the underlying causes of these diseases. CNS disorders are marked by impairments in neurocognitive and neuromuscular functions, and cognitive processes like learning and memory. This deterioration not only impacts the quality of life of affected individuals but also places a significant burden on their families. Neuroplasticity is a key property of the nervous system that enables brain repair and functional recovery. However, in CNS disorders, neuroplasticity is often compromised. Neuroplasticity, which is regulated by gene expression, is also modulated by environmental factors and epigenetic mechanisms, thereby reshaping neuronal networks in response to various biological and environmental stimuli and brain function. Importantly, neuroplasticity plays a critical role in repairing the brain, especially in the context of neurodegenerative diseases, where damaged neurons can reorganize and re-establish lost functions. Targeting neuroplasticity mechanisms holds significant potential for developing therapeutic interventions to improve treatment outcomes and prevent CNS disorders. A deeper understanding of neuroplasticity in neurological diseases could open new avenues for enhancing patient quality of life. This review aims to provide a comprehensive overview of synaptic function and the neuroplasticity mechanisms that are disrupted in neurological disorders.
中枢神经系统(CNS)疾病,如阿尔茨海默病(AD)、帕金森病(PD)、多发性硬化症(MS)和偏头痛,是全球最普遍且令人担忧的疾病之一。尽管研究不断,但这些疾病的病理生理学仍未完全了解,主要原因是其病因复杂。目前的药物治疗主要侧重于缓解症状,而非解决这些疾病的根本原因。中枢神经系统疾病的特征是神经认知和神经肌肉功能受损,以及学习和记忆等认知过程受损。这种恶化不仅影响患者的生活质量,也给其家庭带来巨大负担。神经可塑性是神经系统的关键特性,能够实现大脑修复和功能恢复。然而,在中枢神经系统疾病中,神经可塑性常常受到损害。神经可塑性受基因表达调控,也受环境因素和表观遗传机制调节,从而在响应各种生物和环境刺激及大脑功能时重塑神经网络。重要的是,神经可塑性在大脑修复中起关键作用,尤其是在神经退行性疾病的背景下,受损神经元可以重新组织并恢复失去的功能。针对神经可塑性机制开发治疗干预措施,对于改善治疗效果和预防中枢神经系统疾病具有巨大潜力。更深入地了解神经疾病中的神经可塑性,可能为提高患者生活质量开辟新途径。本综述旨在全面概述神经疾病中被破坏的突触功能和神经可塑性机制。