ReviewFrontiers in aging neuroscience2025
Astaxanthin as a neuroprotective modulator of synaptic plasticity, learning, and memory: mechanistic insights and therapeutic perspectives in neurodegenerative aging.
Review in Frontiers in aging neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed, 1 synthesis or guideline pooled it.
- Efficacy of antioxidants as a therapy for Alzheimer's disease: a meta-analysis.Frontiers in nutrition · 2026Pooled it
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.