中国神经再生研究(英文版) ›› 2023, Vol. 18 ›› Issue (8): 1721-1722.doi: 10.4103/1673-5374.363834

• 观点:退行性病与再生 • 上一篇    下一篇

EAAT2作为阿尔茨海默病的治疗研究靶点:系统评价

  

  1. 脑研究中心,解剖学和医学影像系,医学与健康科学学院,奥克兰大学,新西兰;药理学和治疗学,医学院,戈尔韦神经科学中心,戈尔韦大学,爱尔兰
  • 出版日期:2023-08-15 发布日期:2023-02-23

Is EAAT2 a potential  therapeutic intervention target for Alzheimer’s disease?

Oliver WG Wood, Jason HY Yeung, Andrea Kwakowsky*   

  1. Centre for Brain Research, Department of Anatomy and Medical Imaging, Faculty of Medical and Health Sciences, University of Auckland, Auckland, New Zealand (Wood OWG, Yeung JHY, Kwakowsky A)
    Pharmacology and Therapeutics, School of Medicine, Galway Neuroscience Centre, Ollscoil na Gaillimhe -University of Galway, Galway, Ireland (Kwakowsky A)
  • Online:2023-08-15 Published:2023-02-23
  • Contact: Andrea Kwakowsky, PhD, andrea.kwakowsky@universityofgalway.ie.

摘要: https://orcid.org/0000-0002-3801-4956 (Andrea Kwakowsky)

Abstract: Alzheimer’s disease (AD) is the most common form of dementia worldwide, impairing memory and cognitive functions due to widespread neuronal death. The global incidence of this neurodegenerative disorder is predicted to increase rapidly in the near future. This growth in prevalence of AD will create a large burden for health systems worldwide. Further research into new therapeutic avenues is therefore crucial, given the extremely limited treatment options currently available for AD. The dysfunction and aggregation of two proteins, amyloid-beta (Aβ) and tau, are typically considered the main pathological hallmarks that cause neuronal death in AD. However, numerous other cellular alterations occur, one of which is extensive damage to neurotransmitter systems. Glutamate is the primary excitatory neurotransmitter in the central nervous system and is responsible for the vast majority of excitatory neuron-to-neuron communication throughout the brain. Various receptors, enzymes, and transporters function together in a well-orchestrated manner to ensure glutamatergic homeostasis. The proper regulation of this system is critical for a normal cellular physiological state, given excess activation of glutamatergic postsynaptic receptors can cause glutamate excitotoxicity, which is heavily implicated in the pathogenesis of AD (Han et al., 2016; Yeung et al., 2021).