Targeting the core of neurodegeneration: FoxO, mTOR, and SIRT1

Sep 28, 2020Neural regeneration research

Key Brain Cell Pathways Involved in Neurodegeneration: FoxO, mTOR, and SIRT1

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Abstract

By 2030, treatment services for cognitive disorders in the United States may exceed $2 trillion annually.

An increase in lifespan is associated with a rise in non-communicable diseases, particularly neurodegenerative disorders.
Current treatment options for neurodegenerative disorders do not halt disease progression.
Key cellular mechanisms, including certain transcription factors and pathways, may offer potential strategies for addressing these disorders.
Pathways like autophagy and apoptosis are linked through signaling mechanisms that could enhance neuronal survival and reduce toxic accumulations.
Under specific conditions, these pathways may also lead to cellular death, highlighting the complexity of their roles in treatment.

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The global increase in lifespan noted not only in developed nations, but also in large developing countries parallels an observed increase in a significant number of non-communicable diseases, most notable neurodegenerative disorders. Neurodegenerative disorders present a number of challenges for treatment options that do not resolve disease progression. Furthermore, it is believed by the year 2030, the services required to treat cognitive disorders in the United States alone will exceed $2 trillion annually. Mammalian forkhead transcription factors, silent mating type information regulation 2 homolog 1 (Saccharomyces cerevisiae), the mechanistic target of rapamycin, and the pathways of autophagy and apoptosis offer exciting avenues to address these challenges by focusing upon core cellular mechanisms that may significantly impact nervous system disease. These pathways are intimately linked such as through cell signaling pathways involving protein kinase B and can foster, sometimes in conjunction with trophic factors, enhanced neuronal survival, reduction in toxic intracellular accumulations, and mitochondrial stability. Feedback mechanisms among these pathways also exist that can oversee reparative processes in the nervous system. However, mammalian forkhead transcription factors, silent mating type information regulation 2 homolog 1, mechanistic target of rapamycin, and autophagy can lead to cellular demise under some scenarios that may be dependent upon the precise cellular environment, warranting future studies to effectively translate these core pathways into successful clinical treatment strategies for neurodegenerative disorders.

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Targeting the core of neurodegeneration: FoxO, mTOR, and SIRT1

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