A model of lipid dysregulation and altered nutrient status in Alzheimer's disease
| Autor: | Keith Fluegge |
|---|---|
| Rok vydání: | 2019 |
| Předmět: |
0301 basic medicine
Folate medicine.medical_specialty Disease Choline Dynorphin 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Internal medicine medicine Genetic predisposition Vitamin B12 Phospholipids Nitrous oxide business.industry Theoretical Article Lipid metabolism Environmental exposure Alzheimer's disease Pathophysiology Psychiatry and Mental health Metabolic pathway 030104 developmental biology Endocrinology chemistry Neurology (clinical) business 030217 neurology & neurosurgery |
| Zdroj: | Alzheimer's & Dementia : Translational Research & Clinical Interventions |
| ISSN: | 2352-8737 |
| DOI: | 10.1016/j.trci.2019.03.002 |
| Popis: | Introduction Dysregulated lipid metabolism and nutrient status are thought to play a role in the pathophysiology of Alzheimer's disease (AD). However, the precise involvement is not well understood, and it remains unclear exactly how such dysregulated lipid metabolism and altered nutrient status, especially changes in phosphatidylcholine, B12, and folate, are connected to the hallmark pathology in AD (i.e., amyloidogenesis). Methods We have postulated that genetic susceptibility (i.e., APOE e4/e4) to environmental exposure to emissions of nitrous oxide (N2O) could underlie the onset of AD and its early neuropsychiatric correlates Results and Discussion The current theoretical editorial describes, using clinical, preclinical, and in vitro evidences, how this model contributes not only to amyloidogenesis but also other nonopioid effects, specifically altered lipid metabolism, depletion of vitamin B12, and disruption of the folate-mediated one carbon metabolic pathway. |
| Databáze: | OpenAIRE |
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