ArticleMolecular biology reports2026
Neuroprotective potential of marine-derived polysaccharide against Aβ42-induced toxicity in a Drosophila Alzheimer's disease model.
Article in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundAlzheimer's disease (AD) is a neurodegenerative condition caused by amyloid β (Aβ42) accumulation, neuroinflammation, oxidative stress and cholinergic dysfunction, resulting in neuronal death and cognitive decline. Excessive Aβ42 accumulation disrupts redox equilibrium, increases reactive oxygen species (ROS), and activates inflammatory and apoptotic pathways. Natural bioactive compounds with immunomodulatory and antioxidant properties are increasingly being explored as possible multi-target therapies. Alkylglycerol (AKG), a lipid-derived immunomodulator, and fucoidan, a sulfated polysaccharide found in brown algae, have both shown neuroprotective properties. This study examines the effectiveness of Fucoidan and AKG in preventing Aβ42-induced diseases in a Drosophila melanogaster model, both individually and in combination. METHODOLOGY: Transgenic Drosophila expressing human Aβ42 in the brain were divided into control, Aβ42, Fucoidan-treated, AKG-treated, and combination-treated groups. Oxidative stress indicators such as nitric oxide (NO), hydrogen peroxide (H2O₂), malondialdehyde (MDA), and total ROS were measured using biochemical tests. To evaluate redox reactions, the activity of the antioxidant enzymes glutathione (GSH), catalase (CAT), and superoxide dismutase (SOD) were evaluated. Cholinergic function was assessed by measuring acetylcholinesterase (AChE) activity. The analysis of gene expression focused on genes linked with oxidative stress (SOD, CAT, PHPGx, TRx1), inflammatory markers (TNFα, TNFαR), apoptotic regulator p53, and neurogenesis-related genes (Wnt pathway, SOX2, Nanog). RESULTS AND DISCUSSION: Aβ42 expression disrupted neurogenic signaling and cholinergic balance while markedly increasing oxidative markers and inflammatory mediators. Although AKG and fucoidan separately decreased inflammation and oxidative stress, the combination treatment yielded the biggest results. Dual therapy increased the activity of antioxidant enzymes, decreased the activity of AChE, downregulated TNFα and p53, and restored the expression of Wnt, SOX2, and Nanog. These results demonstrate the translational potential of Fucoidan and AKG act for AD care by showing that their combined treatment helps to restore redox stability, suppress inflammation, boost neurogenesis, and mitigate Aβ42-induced neurotoxicity.
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