Background: With the global increase in lifespan expectancy, neurodegenerative disorders continue to affect an ever-increasing number of individuals throughout the world. New treatment strategies for neurodegenerative diseases are desperately required given the lack of current treatment modalities.
Methods: Here, we examine novel strategies for neurodegenerative disorders that include circadian clock genes, non-coding Ribonucleic Acids (RNAs), and the mammalian forkhead transcription factors of the O class (FoxOs).
Results: Circadian clock genes, non-coding RNAs, and FoxOs offer exciting prospects to potentially limit or remove the significant disability and death associated with neurodegenerative disorders. Each of these pathways has an intimate relationship with the programmed death pathways of autophagy and apoptosis and share a common link to the silent mating type information regulation 2 homolog 1 (Saccharomyces cerevisiae) (SIRT1) and the mechanistic target of rapamycin (mTOR). Circadian clock genes are necessary to modulate autophagy, limit cognitive loss, and prevent neuronal injury. Non-coding RNAs can control neuronal stem cell development and neuronal differentiation and offer protection against vascular disease such as atherosclerosis. FoxOs provide exciting prospects to block neuronal apoptotic death and to activate pathways of autophagy to remove toxic accumulations in neurons that can lead to neurodegenerative disorders.
Conclusion: Continued work with circadian clock genes, non-coding RNAs, and FoxOs can offer new prospects and hope for the development of vital strategies for the treatment of neurodegenerative diseases. These innovative investigative avenues have the potential to significantly limit disability and death from these devastating disorders.
Keywords: Aging, aging-related disorders, Alzheimer's disease, apoptosis, autophagy, BMAL1, cell longevity, circadian rhythm, circular RNA, CLOCK, clock genes, Cryptochrome, deoxyribonucleic acid, diabetes mellitus, erythropoietin, forkhead, FoxO, Huntington’s disease, metabolism, microRNA, mitochondria, mechanistic target of rapamycin (mTOR), non-coding RNA, oxidative stress, Parkinson's disease, period (PER), programmed cell death, REV-ERBα, RORα, RORE, silent mating type information regulation 2 homolog 1 (Saccharomyces cerevisiae) (SIRT1), sirtuin, stem cells, transcription factors, vascular disease.