中国神经再生研究(英文版) ›› 2021, Vol. 21 ›› Issue (5): 1993-1994.doi: 10.4103/NRR.NRR-D-24-01582

• 观点:退行性病与再生 • 上一篇    下一篇

体外微电极阵列在阿尔茨海默病研究中的潜力

  

  • 出版日期:2026-05-15 发布日期:2025-08-22

Potential of in vitro microelectrode arrays in Alzheimer’s disease research

Aoife O’Connell, Andrea Kwakowsky*   

  1. Pharmacology and Therapeutics, School of Medicine, Galway Neuroscience Center, University of Galway, Galway, Ireland
  • Online:2026-05-15 Published:2025-08-22
  • 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 a progressive neurodegenerative disorder and is the most prominent cause of dementia. In 2019, over 57.4 million people were living with AD and other dementia subtypes, a number which is expected to increase to over 152.8 million in the next 25 years. This ever-increasing burden has resulted in AD and other neurodegenerative diseases rising to one of the top 10 causes of death globally (O’Connell et al., 2024). The most wellestablished pathological features of AD include brain shrinkage, accumulation of amyloid-β (Aβ) plaques, neurofibrillary tangles, and a disrupted neuronal network (O’Connell et al., 2024). To date, the cause of AD remains relatively elusive. A plethora of evidence has established Aβ at the forefront of AD pathology, however, the specific mechanisms by which this neurotoxic protein results in the debilitating cognitive decline characteristic of AD remains unknown. It is wellaccepted that the excitatory glutamate and cholinergic neurotransmitter systems are severely altered in AD. More recently, evidence has emerged indicating that the disease also affects the inhibitory GABAergic neurotransmitter system (Govindpani et al., 2017; O’Connell et al., 2024). The molecular changes and neuronal loss in these systems disrupt the excitatory/inhibitory balance in the AD brain, potentially contributing to the memory and learning deficits that characterize the condition (Govindpani et al., 2017).