Metabolic Dysfunction in Parkinson’s Disease: Unraveling the Glucose–Lipid Connection
Despite many years of research into the complex neurobiology of Parkinson’s disease, the precise aetiology cannot be pinpointed down to one causative agent but rather a multitude of mechanisms. Current treatment options can alleviate symptomsbut only slightly slow down the progression and not cure t...
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MDPI AG
2024-12-01
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| author | Jeswinder Sian-Hulsmann Peter Riederer Tanja Maria Michel |
| author_facet | Jeswinder Sian-Hulsmann Peter Riederer Tanja Maria Michel |
| author_sort | Jeswinder Sian-Hulsmann |
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| description | Despite many years of research into the complex neurobiology of Parkinson’s disease, the precise aetiology cannot be pinpointed down to one causative agent but rather a multitude of mechanisms. Current treatment options can alleviate symptomsbut only slightly slow down the progression and not cure the disease and its underlying causes. Factors that play a role in causing the debilitating neurodegenerative psycho-motoric symptoms include genetic alterations, oxidative stress, neuroinflammation, general inflammation, neurotoxins, iron toxicity, environmental influences, and mitochondrial dysfunction. Recent findings suggest that the characteristic abnormal protein aggregation of alpha-synuclein and destruction of substantia nigra neurons might be due to mitochondrial dysfunction related to disturbances in lipid and glucose metabolism along with insulin resistance. The latter mechanism of action might be mediated by insulin receptor substrate docking to proteins that are involved in neuronal survival and signaling related to cell destruction. The increased risk of developing Type 2 Diabetes Mellitus endorses a connection between metabolic dysfunction and neurodegeneration. Here, we explore and highlight the potential role of glycolipid cellular insults in the pathophysiology of the disorder, opening up new promising avenues for the treatment of PD. Thus, antidiabetic drugs may be employed as neuromodulators to hinder the progression of the disorder. |
| format | Article |
| id | doaj-art-41ebcef9d8704367af43078e7fb27a6c |
| institution | DOAJ |
| issn | 2227-9059 |
| language | English |
| publishDate | 2024-12-01 |
| publisher | MDPI AG |
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| series | Biomedicines |
| spelling | doaj-art-41ebcef9d8704367af43078e7fb27a6c2025-08-20T02:53:23ZengMDPI AGBiomedicines2227-90592024-12-011212284110.3390/biomedicines12122841Metabolic Dysfunction in Parkinson’s Disease: Unraveling the Glucose–Lipid ConnectionJeswinder Sian-Hulsmann0Peter Riederer1Tanja Maria Michel2Department of Human Anatomy and Medical Physiology, University of Nairobi, P.O. Box 30197, Nairobi 00100, KenyaResearch Unit of Psychiatry, Department of Psychiatry, Odense, Region of Southern Denmark, University Hospital of Southern Denmark, 5000 Odense, DenmarkResearch Unit of Psychiatry, Department of Psychiatry, Odense, Region of Southern Denmark, University Hospital of Southern Denmark, 5000 Odense, DenmarkDespite many years of research into the complex neurobiology of Parkinson’s disease, the precise aetiology cannot be pinpointed down to one causative agent but rather a multitude of mechanisms. Current treatment options can alleviate symptomsbut only slightly slow down the progression and not cure the disease and its underlying causes. Factors that play a role in causing the debilitating neurodegenerative psycho-motoric symptoms include genetic alterations, oxidative stress, neuroinflammation, general inflammation, neurotoxins, iron toxicity, environmental influences, and mitochondrial dysfunction. Recent findings suggest that the characteristic abnormal protein aggregation of alpha-synuclein and destruction of substantia nigra neurons might be due to mitochondrial dysfunction related to disturbances in lipid and glucose metabolism along with insulin resistance. The latter mechanism of action might be mediated by insulin receptor substrate docking to proteins that are involved in neuronal survival and signaling related to cell destruction. The increased risk of developing Type 2 Diabetes Mellitus endorses a connection between metabolic dysfunction and neurodegeneration. Here, we explore and highlight the potential role of glycolipid cellular insults in the pathophysiology of the disorder, opening up new promising avenues for the treatment of PD. Thus, antidiabetic drugs may be employed as neuromodulators to hinder the progression of the disorder.https://www.mdpi.com/2227-9059/12/12/2841Parkinson’s diseasesubstantia nigraneurodegenerationglucose metabolismlipid metabolismmitochondria |
| spellingShingle | Jeswinder Sian-Hulsmann Peter Riederer Tanja Maria Michel Metabolic Dysfunction in Parkinson’s Disease: Unraveling the Glucose–Lipid Connection Biomedicines Parkinson’s disease substantia nigra neurodegeneration glucose metabolism lipid metabolism mitochondria |
| title | Metabolic Dysfunction in Parkinson’s Disease: Unraveling the Glucose–Lipid Connection |
| title_full | Metabolic Dysfunction in Parkinson’s Disease: Unraveling the Glucose–Lipid Connection |
| title_fullStr | Metabolic Dysfunction in Parkinson’s Disease: Unraveling the Glucose–Lipid Connection |
| title_full_unstemmed | Metabolic Dysfunction in Parkinson’s Disease: Unraveling the Glucose–Lipid Connection |
| title_short | Metabolic Dysfunction in Parkinson’s Disease: Unraveling the Glucose–Lipid Connection |
| title_sort | metabolic dysfunction in parkinson s disease unraveling the glucose lipid connection |
| topic | Parkinson’s disease substantia nigra neurodegeneration glucose metabolism lipid metabolism mitochondria |
| url | https://www.mdpi.com/2227-9059/12/12/2841 |
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