From Clinical to Basic Research: The Neuroprotective Effects and Mechanisms of Caffeine

Review From Clinical to Basic Research: The Neuroprotective Effects and Mechanisms of Caffeine Lijing Wang and Linxi Wang * Department of Endocrinology and Metabolism, Fujian Institute of Endocrinology, Fujian Medical University Union Hospital, Fuzhou 350001, China * Correspondence: [email protected] Received: 15 October 2024; Revised: 31 October 2024; Accepted: 21 February 2025; Published: 1 April 2025 Abstract: Caffeine is the most widely used psychoactive substance in the world, is present in various beverages such as coffee, tea, and energy drinks. Its basic chemical structure contains methylxanthine active components. As a non-selective central adenosine receptor antagonist, caffeine exerts a broad range of pharmacological effects, including antioxidant, anti-inflammatory, and neuroprotective functions. Epidemiological studies and clinical reports suggest that caffeine consumption is closely associated with a reduced risk of neurodegenerative diseases including Alzheimer’s disease, Parkinson’s disease, and dementia. Additionally, caffeine has shown potential benefits in regulating cognitive function, improving depressive symptoms, and reducing the risk of stroke. Although the neuroprotective mechanisms of caffeine remain unclear, current research has revealed that it exerts its effects through multiple signaling pathways, including the inhibition of adenosine A2A receptors, the suppression of neuroinflammation, and the modulation of synaptic plasticity. This paper discusses the recent advancements in research on the neuroprotective effects of caffeine and explores its potential mechanisms and applications in Alzheimer’s disease, Parkinson’s disease, stroke, and depression.