Undaria pinnatifida fucoidan (UPF), a sulphated polysaccharide derived from brown seaweed, has attracted scientific and clinical interest for its wide-ranging anti-inflammatory and neurodegenerative properties. A growing body of research shows that UPF inhibits NF-κB and MAPK signalling pathways, reduces pro-inflammatory cytokines (TNF-α, IL-1β, IL-6), decreases ROS production, and suppresses iNOS and COX-2 activity, thereby mitigating oxidative and inflammatory damage in vitro. In vivo studies confirm these actions, demonstrating reduced systemic inflammation, promoted antioxidant defence, modulated gut microbiota composition, and improved production of beneficial microbial metabolites. In parallel, emerging evidence highlights UPF’s neuroprotective potential, characterised by protection against neuroinflammation and oxidative stress, the attenuation of amyloid-beta deposition, and improvement in neuronal function. Importantly, low- to medium-molecular-weight and highly sulphated UPF fractions consistently exhibit stronger bioactivities, suggesting a structural basis for its therapeutic potential. This review integrates mechanistic evidence from cellular, preclinical, and emerging clinical studies, highlighting UPF as a versatile marine-derived agent with therapeutic relevance for inflammatory and neurodegenerative diseases, and outlines future research directions toward clinical translation.

Undaria pinnatifida fucoidan (UPF), a sulphated polysaccharide derived from brown seaweed, has attracted increasing scientific interest for its wide-ranging anti-inflammatory and neuroprotective properties. Previous studies have demonstrated that UPF exerts significant anti-inflammatory effects through the downregulation of pro-inflammatory cytokines, inhibition of key signalling pathways such as NF-κB and MAPKs, suppression of oxidative stress, and modulation of immune mediators and gut microbiota. In parallel, emerging evidence highlights UPF's neuroprotective potential, characterised by reduced neuroinflammation, oxidative damage, and amyloid-beta accumulation, alongside enhanced antioxidant defence and neuronal function. Current investigations reinforce these findings, suggesting that UPF may serve as a valuable adjunct in managing inflammation-related disorders and neurodegenerative conditions. This review summarises the current knowledge on UPF’s mechanisms of action, with a particular focus on its anti-inflammatory and neuroprotective pathways and implications for brain health, while also identifying gaps for future research and clinical translation.