Alzheimer’s disease (AD) is a progressive neurodegenerative disorder marked by cognitive impairment, memory loss, and behavioural changes. AD is caus

Rotenone, the inhibitor of mitochondrial complex I, is widely used to develop the experimental models of Parkinson’s disease, but the mechanism of neurotoxicity of rotenone is still not clearly established. In the current study we showed that rotenone mediated mitochondrial dysfunctions and cell death in SH-SY5Y cells (human neuroblastoma cell line) over an incubation period of 48 h are triggered by the accumulation of α-synuclein, and silencing of α-synuclein protein expression by specific siRNA abolished the cytotoxic effects of rotenone. Based on the current and earlier published data, the deleterious action of α-synuclein in SH-SY5Y cells has been ascribed to the activation of mitochondrial permeability transition pore (mPTP). In rotenone induced rat model of Parkinson’s disease, nigral dopaminergic neuronal death and altered functions of isolated midbrain mitochondria such as mitochondrial membrane depolarization, decreased ATP synthesis, increased ROS production and inhibition of complex I-III were observed which could be prevented markedly (except complex I-III inhibition) by cyclosporine A which is a well-known blocker of mPTP. The nigral accumulation of α-synuclein after rotenone treatment of rats, however, was not noticeably prevented by cyclosporine A. Additionally, cyclosporine A prevented neuroinflammation in the midbrain region of rotenone treated rats. These results have implications in the pathogenesis and also highlight the therapeutic potential of cyclosporine A for Parkinson’s disease.

Microalgae, a diverse group of photosynthetic microorganisms, have emerged as a promising source of bioactive compounds with significant therapeutic potential. While extensively studied for their applications in nutrition, biofuels, and cosmetics, their role in immunomodulation, particularly in cancer therapy, remains underexplored. This review delves into the intricate relationship between the immune system and cancer, emphasizing the dual role of immune surveillance and immune escape in tumor progression. We highlight the unique potential of microalgae-derived metabolites such as phycocyanin from Spirulina platensis, sulfated polysaccharides from Porphyridium cruentum, fucoxanthin from Phaeodactylum tricornutum, and eicosapentaenoic acid (EPA) from Nannochloropsis spp. in enhancing anti-tumor immunity, modulating the tumor microenvironment, and overcoming immune suppression. These compounds have demonstrated preclinical efficacy in activating macrophages, promoting dendritic cell maturation, stimulating cytotoxic T lymphocytes, and enhancing natural killer (NK) cell activity. Unlike conventional immunotherapies, which often induce adverse effects and resistance, these compounds offer a dual action potential as they exhibit direct antitumor and immune activation properties. In addition to this, algal compounds are natural, potentially less toxic alternatives with multi-targeted immunomodulatory effects. This review stands apart from existing literature by comprehensively integrating insights into cancer immune-editing with the emerging role of microalgae in immune-based therapies. We suggest microalgae as a novel and sustainable approach for upcoming cancer immunotherapy research and chemical application by bridging the gap between marine biotechnology and oncology.