Cellular Metabolism: A Fundamental Component of Degeneration in the Nervous System
It is estimated that, at minimum, 500 million individuals suffer from cellular metabolic dysfunction, such as diabetes mellitus (DM), throughout the world. Even more concerning is the knowledge that metabolic disease is intimately tied to neurodegenerative disorders, affecting both the central and p...
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| Format: | Article |
| Language: | English |
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MDPI AG
2023-05-01
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| Series: | Biomolecules |
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| Online Access: | https://www.mdpi.com/2218-273X/13/5/816 |
| _version_ | 1797600831735857152 |
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| author | Kenneth Maiese |
| author_facet | Kenneth Maiese |
| author_sort | Kenneth Maiese |
| collection | DOAJ |
| description | It is estimated that, at minimum, 500 million individuals suffer from cellular metabolic dysfunction, such as diabetes mellitus (DM), throughout the world. Even more concerning is the knowledge that metabolic disease is intimately tied to neurodegenerative disorders, affecting both the central and peripheral nervous systems as well as leading to dementia, the seventh leading cause of death. New and innovative therapeutic strategies that address cellular metabolism, apoptosis, autophagy, and pyroptosis, the mechanistic target of rapamycin (mTOR), AMP activated protein kinase (AMPK), growth factor signaling with erythropoietin (EPO), and risk factors such as the apolipoprotein E (APOE-ε4) gene and coronavirus disease 2019 (COVID-19) can offer valuable insights for the clinical care and treatment of neurodegenerative disorders impacted by cellular metabolic disease. Critical insight into and modulation of these complex pathways are required since mTOR signaling pathways, such as AMPK activation, can improve memory retention in Alzheimer’s disease (AD) and DM, promote healthy aging, facilitate clearance of β-amyloid (Aß) and tau in the brain, and control inflammation, but also may lead to cognitive loss and long-COVID syndrome through mechanisms that can include oxidative stress, mitochondrial dysfunction, cytokine release, and APOE-ε4 if pathways such as autophagy and other mechanisms of programmed cell death are left unchecked. |
| first_indexed | 2024-03-11T03:54:31Z |
| format | Article |
| id | doaj.art-336b23aadaf946a9b0fd3efac2deb4cf |
| institution | Directory Open Access Journal |
| issn | 2218-273X |
| language | English |
| last_indexed | 2024-03-11T03:54:31Z |
| publishDate | 2023-05-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Biomolecules |
| spelling | doaj.art-336b23aadaf946a9b0fd3efac2deb4cf2023-11-18T00:39:37ZengMDPI AGBiomolecules2218-273X2023-05-0113581610.3390/biom13050816Cellular Metabolism: A Fundamental Component of Degeneration in the Nervous SystemKenneth Maiese0Cellular and Molecular Signaling, New York, NY 10022, USAIt is estimated that, at minimum, 500 million individuals suffer from cellular metabolic dysfunction, such as diabetes mellitus (DM), throughout the world. Even more concerning is the knowledge that metabolic disease is intimately tied to neurodegenerative disorders, affecting both the central and peripheral nervous systems as well as leading to dementia, the seventh leading cause of death. New and innovative therapeutic strategies that address cellular metabolism, apoptosis, autophagy, and pyroptosis, the mechanistic target of rapamycin (mTOR), AMP activated protein kinase (AMPK), growth factor signaling with erythropoietin (EPO), and risk factors such as the apolipoprotein E (APOE-ε4) gene and coronavirus disease 2019 (COVID-19) can offer valuable insights for the clinical care and treatment of neurodegenerative disorders impacted by cellular metabolic disease. Critical insight into and modulation of these complex pathways are required since mTOR signaling pathways, such as AMPK activation, can improve memory retention in Alzheimer’s disease (AD) and DM, promote healthy aging, facilitate clearance of β-amyloid (Aß) and tau in the brain, and control inflammation, but also may lead to cognitive loss and long-COVID syndrome through mechanisms that can include oxidative stress, mitochondrial dysfunction, cytokine release, and APOE-ε4 if pathways such as autophagy and other mechanisms of programmed cell death are left unchecked.https://www.mdpi.com/2218-273X/13/5/816Alzheimer’s diseaseapolipoprotein E (APOE-ε4)AMP activated protein kinase (AMPK)autophagydementiadiabetes mellitus |
| spellingShingle | Kenneth Maiese Cellular Metabolism: A Fundamental Component of Degeneration in the Nervous System Biomolecules Alzheimer’s disease apolipoprotein E (APOE-ε4) AMP activated protein kinase (AMPK) autophagy dementia diabetes mellitus |
| title | Cellular Metabolism: A Fundamental Component of Degeneration in the Nervous System |
| title_full | Cellular Metabolism: A Fundamental Component of Degeneration in the Nervous System |
| title_fullStr | Cellular Metabolism: A Fundamental Component of Degeneration in the Nervous System |
| title_full_unstemmed | Cellular Metabolism: A Fundamental Component of Degeneration in the Nervous System |
| title_short | Cellular Metabolism: A Fundamental Component of Degeneration in the Nervous System |
| title_sort | cellular metabolism a fundamental component of degeneration in the nervous system |
| topic | Alzheimer’s disease apolipoprotein E (APOE-ε4) AMP activated protein kinase (AMPK) autophagy dementia diabetes mellitus |
| url | https://www.mdpi.com/2218-273X/13/5/816 |
| work_keys_str_mv | AT kennethmaiese cellularmetabolismafundamentalcomponentofdegenerationinthenervoussystem |