中国神经再生研究(英文版) ›› 2023, Vol. 18 ›› Issue (7): 1450-1456.doi: 10.4103/1673-5374.360264

• 综述:神经损伤修复保护与再生 • 上一篇    下一篇

环境富集对帕金森病的神经保护分子机制

  


  • 出版日期:2023-07-15 发布日期:2023-01-11

Molecular mechanisms underlying the neuroprotection of environmental enrichment in Parkinson’s disease

Tamara Andrea Alarcón1, 2, Sarah Martins Presti-Silva2, 3, Ana Paula Toniato Simões1, 2, Fabiola Mara Ribeiro3, *, Rita Gomes Wanderley Pires1, 2, *#br#   

  1. 1Department of Physiological Sciences, Health Science Center, Universidade Federal do Espirito Santo, Vitoria, Brazil; 2Laboratory of Molecular and Behavioral Neurobiology, Health Science Center, Universidade Federal do Espirito Santo, Vitoria, Brazil; 3Department of Biochemistry and Immunology, Institute o Biological Sciences, Universidade Federal de Minas Gerais, Avenida Antônio Carlos, Belo Horizonte, Brazil
  • Online:2023-07-15 Published:2023-01-11
  • Contact: Fabiola Mara Ribeiro, PhD, fmribeiro@icb.ufmg.br or rfabiola26@hotmail.com; Rita Gomes Wanderley Pires, PhD, rita.pires@ufes.br.

摘要: https://orcid.org/0000-0001-7042-9433 (Fabiola Mara Ribeiro); https://orcid.org/0000-0002-4739-8349 (Rita Gomes Wanderley Pires)

Abstract: Parkinson’s disease is the most common movement disorder, affecting about 1% of the population over the age of 60 years. Parkinson’s disease is characterized clinically by resting tremor, bradykinesia, rigidity and postural instability, as a result of the progressive loss of nigrostriatal dopaminergic neurons. In addition to this neuronal cell loss, Parkinson’s disease is characterized by the accumulation of intracellular protein aggregates, Lewy bodies and Lewy neurites, composed primarily of the protein α-synuclein. Although it was first described almost 200 years ago, there are no disease-modifying drugs to treat patients with Parkinson’s disease. In addition to conventional therapies, non-pharmacological treatment strategies are under investigation in patients and animal models of neurodegenerative disorders. Among such strategies, environmental enrichment, comprising physical exercise, cognitive stimulus, and social interactions, has been assessed in preclinical models of Parkinson’s disease. Environmental enrichment can cause structural and functional changes in the brain and promote neurogenesis and dendritic growth by modifying gene expression, enhancing the expression of neurotrophic factors and modulating neurotransmission. In this review article, we focus on the current knowledge about the molecular mechanisms underlying environmental enrichment neuroprotection in Parkinson’s disease, highlighting its influence on the dopaminergic, cholinergic, glutamatergic and GABAergic systems, as well as the involvement of neurotrophic factors. We describe experimental pre-clinical data showing how environmental enrichment can act as a modulator in a neurochemical and behavioral context in different animal models of Parkinson’s disease, highlighting the potential of environmental enrichment as an additional strategy in the management and prevention of this complex disease. 

Key words: acetylcholine, brain-derived neurotrophic factor, dopamine, environment enrichment, gamma-aminobutyric acid, glial cell line-derived neurotrophic factor, glutamate, molecular mechanisms, Parkinson’s disease