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High dietary consumption of trans fatty acids decreases brain docosahexaenoic acid but does not alter amyloid-beta and tau pathologies in the 3xTg-AD model of Alzheimer's disease.
Neuroscience 2009; 159(1):296-307N

Abstract

Dietary consumption of trans fatty acids (TFA) has increased during the 20th century and is a suspected risk factor for cardiovascular diseases. More recently, high TFA intake has been associated with a higher risk of developing Alzheimer's disease (AD). To investigate the impact of TFA on an animal model genetically programmed to express amyloid-beta (Abeta) and tau pathological markers of AD, we have fed 3xTg-AD mice with either control (0% TFA/total fatty acid), high TFA (16% TFA) or very high TFA (43% TFA) isocaloric diets from 2 to 16 months of age. Effects of TFA on plasma hepatic enzymes, glucose and lipid profile were minimal but very high TFA intake decreased visceral fat of non-transgenic mice. Importantly, dietary TFA increased brain TFA concentrations in a dose-related manner. Very high TFA consumption substantially modified the brain fatty acid profile by increasing mono-unsaturated fatty acids and decreasing polyunsaturated fatty acids (PUFA). Very high TFA intake induced a shift from docosahexaenoic acid (DHA, 22:6n-3) toward n-6 docosapentaenoic acid (DPA, 22:5n-6) without altering the n-3:n-6 PUFA ratio in the cortex of both control and 3xTg-AD mice. Changes in levels of Abeta(40), Abeta(42), tau protein, phosphorylated tau protein and synaptic markers were not statistically significant in the three groups of 3xTg-AD mice, despite a trend toward decreased insoluble tau in very high TFA-fed 3xTg-AD animals. In summary, TFA intake modulated brain fatty acid profiles but had no significant effect on major brain neuropathological hallmarks of AD in an animal model.

Authors+Show Affiliations

Faculty of Pharmacy, Université Laval, 1050 de la Médecine Avenue, Québec, Québec, Canada G1V 0A6.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

19135506

Citation

Phivilay, A, et al. "High Dietary Consumption of Trans Fatty Acids Decreases Brain Docosahexaenoic Acid but Does Not Alter Amyloid-beta and Tau Pathologies in the 3xTg-AD Model of Alzheimer's Disease." Neuroscience, vol. 159, no. 1, 2009, pp. 296-307.
Phivilay A, Julien C, Tremblay C, et al. High dietary consumption of trans fatty acids decreases brain docosahexaenoic acid but does not alter amyloid-beta and tau pathologies in the 3xTg-AD model of Alzheimer's disease. Neuroscience. 2009;159(1):296-307.
Phivilay, A., Julien, C., Tremblay, C., Berthiaume, L., Julien, P., Giguère, Y., & Calon, F. (2009). High dietary consumption of trans fatty acids decreases brain docosahexaenoic acid but does not alter amyloid-beta and tau pathologies in the 3xTg-AD model of Alzheimer's disease. Neuroscience, 159(1), pp. 296-307. doi:10.1016/j.neuroscience.2008.12.006.
Phivilay A, et al. High Dietary Consumption of Trans Fatty Acids Decreases Brain Docosahexaenoic Acid but Does Not Alter Amyloid-beta and Tau Pathologies in the 3xTg-AD Model of Alzheimer's Disease. Neuroscience. 2009 Mar 3;159(1):296-307. PubMed PMID: 19135506.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - High dietary consumption of trans fatty acids decreases brain docosahexaenoic acid but does not alter amyloid-beta and tau pathologies in the 3xTg-AD model of Alzheimer's disease. AU - Phivilay,A, AU - Julien,C, AU - Tremblay,C, AU - Berthiaume,L, AU - Julien,P, AU - Giguère,Y, AU - Calon,F, Y1 - 2008/12/14/ PY - 2008/09/22/received PY - 2008/12/04/revised PY - 2008/12/06/accepted PY - 2009/1/13/entrez PY - 2009/1/13/pubmed PY - 2009/6/26/medline SP - 296 EP - 307 JF - Neuroscience JO - Neuroscience VL - 159 IS - 1 N2 - Dietary consumption of trans fatty acids (TFA) has increased during the 20th century and is a suspected risk factor for cardiovascular diseases. More recently, high TFA intake has been associated with a higher risk of developing Alzheimer's disease (AD). To investigate the impact of TFA on an animal model genetically programmed to express amyloid-beta (Abeta) and tau pathological markers of AD, we have fed 3xTg-AD mice with either control (0% TFA/total fatty acid), high TFA (16% TFA) or very high TFA (43% TFA) isocaloric diets from 2 to 16 months of age. Effects of TFA on plasma hepatic enzymes, glucose and lipid profile were minimal but very high TFA intake decreased visceral fat of non-transgenic mice. Importantly, dietary TFA increased brain TFA concentrations in a dose-related manner. Very high TFA consumption substantially modified the brain fatty acid profile by increasing mono-unsaturated fatty acids and decreasing polyunsaturated fatty acids (PUFA). Very high TFA intake induced a shift from docosahexaenoic acid (DHA, 22:6n-3) toward n-6 docosapentaenoic acid (DPA, 22:5n-6) without altering the n-3:n-6 PUFA ratio in the cortex of both control and 3xTg-AD mice. Changes in levels of Abeta(40), Abeta(42), tau protein, phosphorylated tau protein and synaptic markers were not statistically significant in the three groups of 3xTg-AD mice, despite a trend toward decreased insoluble tau in very high TFA-fed 3xTg-AD animals. In summary, TFA intake modulated brain fatty acid profiles but had no significant effect on major brain neuropathological hallmarks of AD in an animal model. SN - 0306-4522 UR - https://www.unboundmedicine.com/medline/citation/19135506/High_dietary_consumption_of_trans_fatty_acids_decreases_brain_docosahexaenoic_acid_but_does_not_alter_amyloid_beta_and_tau_pathologies_in_the_3xTg_AD_model_of_Alzheimer's_disease_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0306-4522(08)01762-4 DB - PRIME DP - Unbound Medicine ER -