Adenosine and Its Receptors: Emerging Targets in Neurodegenerative Diseases

A Special Issue of Biomolecules (ISSN 2218-273X) belonging to the section "Molecular Biology".

Deadline for manuscript submissions: 15 December 2026 | Viewed by 226

Editor


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Guest Editor
Department of Medicine, University of California San Diego, La Jolla, CA 92093, USA
Interests: lipid metabolism; metabolic disease; inflammation; signal transduction; neurodegenerative disease; mitochondria; macrophage/microglia biology
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Special Issue Information

Dear Colleagues,

Adenosine is an endogenous purine nucleoside that regulates neuronal activity, inflammation, and energy balance through its receptors (A1, A2A, A2B, and A3). In neurodegenerative diseases such as Alzheimer’s, Parkinson’s, and Huntington’s, dysregulated adenosine signaling contributes to neuronal dysfunction and progression of pathology. A1 receptors generally provide neuroprotective effects by reducing excitotoxicity, while A2A receptor activation is often linked to neuroinflammation and neuronal damage. Targeting adenosine receptors has emerged as a promising therapeutic strategy to modulate neuroinflammation, improve synaptic function, and slow disease progression in neurodegenerative disorders.

This Special Issue aims to present research that provides new insights into the role of adenosine and its receptors in neurodegenerative disorders. Topics of interest include, but are not limited to, molecular mechanisms of adenosine signaling, receptor-specific functions in the central nervous system, interactions with neuroinflammatory pathways, and the development of pharmacological modulators targeting adenosine receptors. We welcome original research articles, reviews, and other types of scholarly contributions. Studies spanning experimental, translational, and preclinical approaches are particularly encouraged.

We look forward to your contributions.

Dr. Soo-Ho Choi
Guest Editor

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Keywords

  • adenosine
  • adenosine receptors
  • neuroinflammation
  • neurodegenerative diseases

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