Astaxanthin as a neuroprotective modulator of synaptic plasticity, learning, and memory: mechanistic insights and therapeutic perspectives in neurodegenerative aging.

Research overview

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Astaxanthin (AST), a xanthophyll carotenoid derived from microalgae and marine organisms, has emerged as a potent neuroprotective compound with remarkable antioxidant and anti-inflammatory properties. Growing evidence indicates that AST can modulate multiple molecular and cellular pathways involved in neuronal survival, synaptic plasticity, learning, and memory, particularly in the context of neurodegenerative aging. This review provides an up-to-date and integrative overview of current evidence regarding AST's mechanisms of action across experimental and preclinical models of neurodegenerative diseases such as Alzheimer's, Parkinson's, and Huntington's diseases. We highlight its role in mitigating oxidative stress, regulating mitochondrial function, modulating neuroinflammatory signaling, and promoting neurogenesis and synaptic remodeling. Furthermore, we discuss how AST influences key molecular pathways that underlie cognitive function and plasticity. The translational potential of AST as a therapeutic and preventive agent is critically evaluated, alongside its pharmacokinetic challenges, bioavailability, and safety profile in aging populations. Finally, we identify current research gaps and propose future directions toward harnessing AST for promoting cognitive resilience and delaying the progression of neurodegenerative disorders. Collectively, the evidence supports AST as a promising candidate for maintaining neuronal health and cognitive function during brain aging.

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