Identification of the abnormalities in astrocytic functions as potential drug targets for neurodegenerative disease

Valtteri Syvänen, Jari Koistinaho, Šárka Lehtonen

Research output: Contribution to journalReview Articlepeer-review

Abstract

Introduction: Historically, astrocytes were seen primarily as a supportive cell population within the brain; with neurodegenerative disease research focusing exclusively on malfunctioning neurons. However, astrocytes perform numerous tasks that are essential for maintenance of the central nervous system`s complex processes. Disruption of these functions can have negative consequences; hence, it is unsurprising to observe a growing amount of evidence for the essential role of astrocytes in the development and progression of neurodegenerative diseases. Targeting astrocytic functions may serve as a potential disease-modifying drug therapy in the future. Areas covered: The present review emphasizes the key astrocytic functions associated with neurodegenerative diseases and explores the possibility of pharmaceutical interventions to modify these processes. In addition, the authors provide an overview of current advancement in this field by including studies of possible drug candidates. Expert opinion: Glial research has experienced a significant renaissance in the last quarter-century. Understanding how disease pathologies modify or are caused by astrocyte functions is crucial when developing treatments for brain diseases. Future research will focus on building advanced models that can more precisely correlate to the state in the human brain, with the goal of routinely testing therapies in these models.

Original languageEnglish
JournalExpert opinion on drug discovery
Volume19
Issue number5
Pages (from-to)603-616
Number of pages14
ISSN1746-0441
DOIs
Publication statusPublished - 2024
MoE publication typeA2 Review article in a scientific journal

Fields of Science

  • BBB
  • neuroinflammation
  • glutamate uptake
  • neurodegeneration
  • Astrocyte
  • oxidative stress
  • 3112 Neurosciences

Cite this