Ferropanoptosis in Neurocysticercosis: Implications for Novel Therapeutic Drug Development: A Comprehensive Review
Author(s): Lourdes de Fatima Ibanez Valdes and Foyaca-Sibat Humberto*
Abstract
Background: Ferroptosis (Fp), a newly reported Regulated Cell Death (RCD) associated with iron independence lipid peroxidation (LP), has become a fundamental process involved in the neuropathological basis in the comorbidity of NCC/COVID-19 and PANoptosis represent a group of different RCD and Programmed Cell Death (PCD) as we reported previously. Taenia solium (Ts), the larval form of the pig tapeworm, is the primary cause of the preventable and eradicable zoonotic parasitic disease Cysticercosis (Ct), which is primarily observed in individuals residing in underdeveloped nations. However, because to unregulated migration and globalization, the number of carriers in wealthy nations is steadily rising. In this investigation, we seek to learn more about the pathophysiology of neuropsychiatric symptoms in individuals suffering from Neurocysticercosis (NPNCC). Drug development strategies aimed at targeting ferropanoptosis in NCC are promising. Potential therapeutic approaches include: Iron chelators: Compounds that sequester iron ions, reducing their availability for catalyzing lipid peroxidation and subsequent cell death.
Antioxidants: Substances that counteract lipid peroxidation and oxidative stress, thereby protecting neurons from ferroptotic damage.
Lipid peroxidation inhibitors: Molecules that inhibit the enzymatic pathways involved in lipid peroxidation, preventing neuronal membrane damage.
Combination therapies: Synergistic approaches combining iron chelators with antioxidants or lipid peroxidation inhibitors to maximize neuroprotective effects.
Recent advances in understanding ferropanoptosis and its role in NCC highlight the potential for personalized medicine approaches tailored to individual patient profiles and disease stages. Future research should focus on clinical trials to validate the efficacy and safety of these novel therapeutic strategies, ultimately improving outcomes and quality of life for NCC patients globally.
Method: Using a comprehensive search strategy, we looked for published medical subject heading (MeSH) terms such as “neurocysticercosis”, “pathophysiology of Fp/NCC”, “immunology of FPANp” OR “dysfunctional mitochondria in FPANp”, “necroptosis/apoptosis/ pyroptosis/autophagia/NCC.”
Results: Peer review was conducted on all of the chosen studies, and we were unable to locate any literature discussing the pathophysiology of FPANp in NCC.
Remarks and closing thoughts: We postulated that the pathophysiology of FPANp in patients with NCC is influenced by malfunctioning mitochondria, oxidative stress, neuroinflammation, Fp, and PANp.
