Cognitive impairment with diabetes mellitus and metabolic disease: innovative insights with the mechanistic target of rapamycin and circadian clock gene pathways

Dec 4, 2019Expert review of clinical pharmacology

Cognitive problems in diabetes and metabolic disease linked to cell growth control and body clock genes

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Abstract

Dementia is the 7th leading cause of death, significantly impacting global health and finances.

Only symptomatic care is currently available for cognitive loss related to conditions like Alzheimer's disease.
Cognitive loss may be associated with metabolic disorders, particularly diabetes mellitus, which affects 350 million people worldwide.
Novel treatment strategies targeting pathways such as mechanistic target of rapamycin (mTOR) and circadian clock genes are being explored for their potential to address cognitive loss.
These pathways, including AMP activated protein kinase (AMPK) and others, could offer new avenues to treat dementia related to metabolic dysfunction.
The complexity of these pathways necessitates careful regulation to enhance treatment effectiveness and reduce clinical risks.

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: Dementia is the 7th leading cause of death that imposes a significant financial and service burden on the global population. Presently, only symptomatic care exists for cognitive loss, such as Alzheimer's disease.: Given the advancing age of the global population, it becomes imperative to develop innovative therapeutic strategies for cognitive loss. New studies provide insight to the association of cognitive loss with metabolic disorders, such as diabetes mellitus.: Diabetes mellitus is increasing in incidence throughout the world and affects 350 million individuals. Treatment strategies identifying novel pathways that oversee metabolic and neurodegenerative disorders offer exciting prospects to treat dementia. The mechanistic target of rapamycin (mTOR) and circadian clock gene pathways that include AMP activated protein kinase (AMPK), Wnt1 inducible signaling pathway protein 1 (WISP1), erythropoietin (EPO), and silent mating type information regulation 2 homolog 1) (SIRT1) provide novel strategies to treat cognitive loss that has its basis in metabolic cellular dysfunction. However, these pathways are complex and require precise regulation to maximize treatment efficacy and minimize any potential clinical disability. Further investigations hold great promise to treat both the onset and progression of cognitive loss that is associated with metabolic disease. Introduction Areas covered Expert opinion (Saccharomyces cerevisiae

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Cognitive impairment with diabetes mellitus and metabolic disease: innovative insights with the mechanistic target of rapamycin and circadian clock gene pathways

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