Walnut Oil Reduces Aβ Levels and Increases Neurite Length in a Cellular Model of Early Alzheimer Disease
(1) Background: Mitochondria are the cells’ main source of energy. Mitochondrial dysfunction represents a key hallmark of aging and is linked to the development of Alzheimer’s disease (AD). Maintaining mitochondrial function might contribute to healthy aging and the prevention of AD. The Mediterrane...
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MDPI AG
2022-04-01
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| Series: | Nutrients |
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| Online Access: | https://www.mdpi.com/2072-6643/14/9/1694 |
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| author | Carsten Esselun Fabian Dieter Nadine Sus Jan Frank Gunter P. Eckert |
| author_facet | Carsten Esselun Fabian Dieter Nadine Sus Jan Frank Gunter P. Eckert |
| author_sort | Carsten Esselun |
| collection | DOAJ |
| description | (1) Background: Mitochondria are the cells’ main source of energy. Mitochondrial dysfunction represents a key hallmark of aging and is linked to the development of Alzheimer’s disease (AD). Maintaining mitochondrial function might contribute to healthy aging and the prevention of AD. The Mediterranean diet, including walnuts, seems to prevent age-related neurodegeneration. Walnuts are a rich source of α-linolenic acid (ALA), an essential n3-fatty acid and the precursor for n3-long-chain polyunsaturated fatty acids (n3-PUFA), which might potentially improve mitochondrial function. (2) Methods: We tested whether a lipophilic walnut extract (WE) affects mitochondrial function and other parameters in human SH-SY5Y cells transfected with the neuronal amyloid precursor protein (APP695). Walnut lipids were extracted using a Soxhlet Extraction System and analyzed using GC/MS and HPLC/FD. Adenosine triphosphate (ATP) concentrations were quantified under basal conditions in cell culture, as well as after rotenone-induced stress. Neurite outgrowth was investigated, as well as membrane integrity, cellular reactive oxygen species, cellular peroxidase activity, and citrate synthase activity. Beta-amyloid (Aβ) was quantified using homogenous time-resolved fluorescence. (3) Results: The main constituents of WE are linoleic acid, oleic acid, α-linolenic acid, and γ- and δ-tocopherol. Basal ATP levels following rotenone treatment, as well as citrate synthase activity, were increased after WE treatment. WE significantly increased cellular reactive oxygen species but lowered peroxidase activity. Membrane integrity was not affected. Furthermore, WE treatment reduced Aβ<sub>1–40</sub> and stimulated neurite growth. (4) Conclusions: WE might increase ATP production after induction of mitochondrial biogenesis. Decreased Aβ<sub>1–40</sub> formation and enhanced ATP levels might enhance neurite growth, making WE a potential agent to enhance neuronal function and to prevent the development of AD. In this sense, WE could be a promising agent for the prevention of AD. |
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| language | English |
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| series | Nutrients |
| spelling | doaj.art-108787a5b39f4cacb26f285b2cabf3f72023-11-23T08:57:05ZengMDPI AGNutrients2072-66432022-04-01149169410.3390/nu14091694Walnut Oil Reduces Aβ Levels and Increases Neurite Length in a Cellular Model of Early Alzheimer DiseaseCarsten Esselun0Fabian Dieter1Nadine Sus2Jan Frank3Gunter P. Eckert4Biomedical Research Center, Institute of Nutritional Sciences, Justus-Liebig-University of Giessen, Schubert-Street 81, D-35392 Giessen, GermanyBiomedical Research Center, Institute of Nutritional Sciences, Justus-Liebig-University of Giessen, Schubert-Street 81, D-35392 Giessen, GermanyDepartment of Food Biofunctionality, Institute of Nutritional Sciences, University of Hohenheim, Ökozentrum, Garbenstr. 28, D-70599 Stuttgart, GermanyDepartment of Food Biofunctionality, Institute of Nutritional Sciences, University of Hohenheim, Ökozentrum, Garbenstr. 28, D-70599 Stuttgart, GermanyBiomedical Research Center, Institute of Nutritional Sciences, Justus-Liebig-University of Giessen, Schubert-Street 81, D-35392 Giessen, Germany(1) Background: Mitochondria are the cells’ main source of energy. Mitochondrial dysfunction represents a key hallmark of aging and is linked to the development of Alzheimer’s disease (AD). Maintaining mitochondrial function might contribute to healthy aging and the prevention of AD. The Mediterranean diet, including walnuts, seems to prevent age-related neurodegeneration. Walnuts are a rich source of α-linolenic acid (ALA), an essential n3-fatty acid and the precursor for n3-long-chain polyunsaturated fatty acids (n3-PUFA), which might potentially improve mitochondrial function. (2) Methods: We tested whether a lipophilic walnut extract (WE) affects mitochondrial function and other parameters in human SH-SY5Y cells transfected with the neuronal amyloid precursor protein (APP695). Walnut lipids were extracted using a Soxhlet Extraction System and analyzed using GC/MS and HPLC/FD. Adenosine triphosphate (ATP) concentrations were quantified under basal conditions in cell culture, as well as after rotenone-induced stress. Neurite outgrowth was investigated, as well as membrane integrity, cellular reactive oxygen species, cellular peroxidase activity, and citrate synthase activity. Beta-amyloid (Aβ) was quantified using homogenous time-resolved fluorescence. (3) Results: The main constituents of WE are linoleic acid, oleic acid, α-linolenic acid, and γ- and δ-tocopherol. Basal ATP levels following rotenone treatment, as well as citrate synthase activity, were increased after WE treatment. WE significantly increased cellular reactive oxygen species but lowered peroxidase activity. Membrane integrity was not affected. Furthermore, WE treatment reduced Aβ<sub>1–40</sub> and stimulated neurite growth. (4) Conclusions: WE might increase ATP production after induction of mitochondrial biogenesis. Decreased Aβ<sub>1–40</sub> formation and enhanced ATP levels might enhance neurite growth, making WE a potential agent to enhance neuronal function and to prevent the development of AD. In this sense, WE could be a promising agent for the prevention of AD.https://www.mdpi.com/2072-6643/14/9/1694walnutpoly-unsaturated fatty acidsPUFAvitamin Emitochondrianeurodegeneration |
| spellingShingle | Carsten Esselun Fabian Dieter Nadine Sus Jan Frank Gunter P. Eckert Walnut Oil Reduces Aβ Levels and Increases Neurite Length in a Cellular Model of Early Alzheimer Disease Nutrients walnut poly-unsaturated fatty acids PUFA vitamin E mitochondria neurodegeneration |
| title | Walnut Oil Reduces Aβ Levels and Increases Neurite Length in a Cellular Model of Early Alzheimer Disease |
| title_full | Walnut Oil Reduces Aβ Levels and Increases Neurite Length in a Cellular Model of Early Alzheimer Disease |
| title_fullStr | Walnut Oil Reduces Aβ Levels and Increases Neurite Length in a Cellular Model of Early Alzheimer Disease |
| title_full_unstemmed | Walnut Oil Reduces Aβ Levels and Increases Neurite Length in a Cellular Model of Early Alzheimer Disease |
| title_short | Walnut Oil Reduces Aβ Levels and Increases Neurite Length in a Cellular Model of Early Alzheimer Disease |
| title_sort | walnut oil reduces aβ levels and increases neurite length in a cellular model of early alzheimer disease |
| topic | walnut poly-unsaturated fatty acids PUFA vitamin E mitochondria neurodegeneration |
| url | https://www.mdpi.com/2072-6643/14/9/1694 |
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