中国神经再生研究(英文版) ›› 2021, Vol. 16 ›› Issue (7): 1399-1401.doi: 10.4103/1673-5374.301009

• 观点:退行性病与再生 • 上一篇    下一篇

β淀粉样蛋白对海马谷氨酸能受体和转运蛋白表达的影响

  

  • 出版日期:2021-07-15 发布日期:2021-01-07

The effects of amyloid-beta on hippocampal glutamatergic receptor and transporter expression

Andrea Kwakowsky*, Henry J. Waldvogel, Richard LM Faull   

  1. Centre for Brain Research, Department of Anatomy and Medical Imaging, Faculty of Medical and Health Sciences, University of Auckland, Auckland, New Zealand
  • Online:2021-07-15 Published:2021-01-07
  • Contact: Andrea Kwakowsky, PhD, a.kwakowsky@auckland.ac.nz.

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

Abstract: The leading form of dementia worldwide, Alzheimer’s disease (AD) is a common neurodegenerative disorder. The underlying causes of AD are not well understood, and no current treatments are preventing the onset or delay progression of the disease. Currently, most investigation is directed towards the amyloid-beta (Aβ) and tau pathologies, yet there are many other underlying processes that have been implicated to contribute directly to AD progression. One such phenomenon is glutamatergic excitotoxicity, a loss of neuromodulatory balance inducing a hyper-excitable neuronal state, leading to cell death across several brain regions (Zhang et al., 2016; Bukke et al., 2020). Glutamate is the primary excitatory neurotransmitter in the brain and is involved in many critical signaling and metabolic functions but control of the glutamatergic system requires constant moderation to avoid excitotoxicity occurring (Bukke et al., 2020). As yet, glutamatergic signaling changes that contribute to this process, or result due to this process, have not been thoroughly investigated.