Title:Novel Treatment Strategies for the Nervous System: Circadian Clock Genes, Non-coding RNAs, and Forkhead Transcription Factors
Volume: 15
Issue: 1
Author(s): Kenneth Maiese*
Affiliation:
- New Jersey Cellular Sciences University, Newark, New Jersey 07101,United States
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.
Abstract: 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.
