Examining the Overlap Between Rejuvenation Mechanisms in Turritopsis dohrnii and Human Neurodegeneration: A Systematic Review
Mariam Ashraf
Raedat AlSalam, Riyadh, Saudi Arabia
Publication date: November 20, 2025
Raedat AlSalam, Riyadh, Saudi Arabia
Publication date: November 20, 2025
DOI: http://doi.org/10.34614/JIYRC2025II53
ABSTRACT
Neurodegenerative diseases are becoming one of the most significant causes of worldwide morbidity. This systematic review explores the intersection between rejuvenation mechanisms in T.dohrnii and neurodegeneration in humans. Turritopsis dohrnii maintains telomerase activation and mitochondrial stability and controls reactive oxygen species during regeneration, whereas human neurons exhibit telomere shortening, mitochondrial dysfunction, and oxidative stress. All these contribute to neuronal decline presented in neurodegenerative diseases such as Alzheimer’s and Parkinson’s. Moreover, transdifferentiation and whole-body regeneration processes distinguish T. dohrnii from most other organisms. Tau accumulation, amyloid-β plaques, and blood-brain barrier disruption are also found in neurodegeneration, not in T. dohrnii. These findings indicate concurrent pathways such as DNA repair, FOXO pathway, mitochondrial stability, and antioxidant protection, but also reveal profound differences. The aim is not to suggest that T. dohrnii holds the cure, but that its biology has implications for protective mechanisms guiding strategies to delay or reduce neurodegeneration.
Neurodegenerative diseases are becoming one of the most significant causes of worldwide morbidity. This systematic review explores the intersection between rejuvenation mechanisms in T.dohrnii and neurodegeneration in humans. Turritopsis dohrnii maintains telomerase activation and mitochondrial stability and controls reactive oxygen species during regeneration, whereas human neurons exhibit telomere shortening, mitochondrial dysfunction, and oxidative stress. All these contribute to neuronal decline presented in neurodegenerative diseases such as Alzheimer’s and Parkinson’s. Moreover, transdifferentiation and whole-body regeneration processes distinguish T. dohrnii from most other organisms. Tau accumulation, amyloid-β plaques, and blood-brain barrier disruption are also found in neurodegeneration, not in T. dohrnii. These findings indicate concurrent pathways such as DNA repair, FOXO pathway, mitochondrial stability, and antioxidant protection, but also reveal profound differences. The aim is not to suggest that T. dohrnii holds the cure, but that its biology has implications for protective mechanisms guiding strategies to delay or reduce neurodegeneration.
