中国神经再生研究(英文版) ›› 2021, Vol. 16 ›› Issue (1): 58-67.doi: 10.4103/1673-5374.286952

• 综述:视神经损伤修复保护与再生 • 上一篇    下一篇

神经可塑性和脑退化机制:衰老过程中的保护策略

  

  • 出版日期:2021-01-15 发布日期:2020-11-23

Mechanisms of neuroplasticity and brain degeneration: strategies for protection during the aging process

Mariana Toricelli1, Arthur Antonio Ruiz Pereira2, Guilherme Souza Abrao2, Helena Nascimento Malerba2, Julia Maia2, Hudson Sousa Buck1, Tania Araujo Viel2, *   

  1. 1 Department of Physiological Sciences, Santa Casa de Sao Paulo School of Medical Sciences, Sao Paulo, Brazil;  2 Laboratory of Neurobiology of Aging, School of Arts, Sciences and Humanities, Universidade de São Paulo, Sao Paulo, Brazil
  • Online:2021-01-15 Published:2020-11-23
  • Contact: Tania Araujo Viel, taniaviel@usp.br.
  • Supported by:
    MT received studentship from Sao Paulo Research Foundation (2017/21655-6). HSB was a Brazilian National Council for Scientific and Technological Development researcher (425838/2016-1, 307252/2017-5). This work was financed in part by the Coordenação de Aperfeiçoamento de Pessoal de Nível Superior – Brasil (CAPES) – Finance Code 001 and FAPESP (2016/07115-6).

摘要: https://orcid.org/0000-0002-4015-785X (Tania Araujo Viel) 

Abstract: Aging is a dynamic and progressive process that begins at conception and continues until death. This process leads to a decrease in homeostasis and morphological, biochemical and psychological changes, increasing the individual’s vulnerability to various diseases. The growth in the number of aging populations has increased the prevalence of chronic degenerative diseases, impairment of the central nervous system and dementias, such as Alzheimer’s disease, whose main risk factor is age, leading to an increase of the number of individuals who need daily support for life activities. Some theories about aging suggest it is caused by an increase of cellular senescence and reactive oxygen species, which leads to inflammation, oxidation, cell membrane damage and consequently neuronal death. Also, mitochondrial mutations, which are generated throughout the aging process, can lead to changes in energy production, deficiencies in electron transport and apoptosis induction that can result in decreased function. Additionally, increasing cellular senescence and the release of proinflammatory cytokines can cause irreversible damage to neuronal cells. Recent reports point to the importance of changing lifestyle by increasing physical exercise, improving nutrition and environmental enrichment to activate neuroprotective defense mechanisms. Therefore, this review aims to address the latest information about the different mechanisms related to neuroplasticity and neuronal death and to provide strategies that can improve neuroprotection and decrease the neurodegeneration caused by aging and environmental stressors.

Key words: cell senescence, cell signaling, cholinergic, enriched environment, long-term potentiation, neurodegeneration, neurogenesis, neuroinflammatory, neuronal death, neuroprotection, neurotophin