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. 2017 Dec 7;7(1):17134.
doi: 10.1038/s41598-017-17373-3.

Effect of Canola Oil Consumption on Memory, Synapse and Neuropathology in the Triple Transgenic Mouse Model of Alzheimer's Disease

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Free PMC article

Effect of Canola Oil Consumption on Memory, Synapse and Neuropathology in the Triple Transgenic Mouse Model of Alzheimer's Disease

Elisabetta Lauretti et al. Sci Rep. .
Free PMC article

Abstract

In recent years consumption of canola oil has increased due to lower cost compared with olive oil and the perception that it shares its health benefits. However, no data are available on the effect of canola oil intake on Alzheimer's disease (AD) pathogenesis. Herein, we investigated the effect of chronic daily consumption of canola oil on the phenotype of a mouse model of AD that develops both plaques and tangles (3xTg). To this end mice received either regular chow or a chow diet supplemented with canola oil for 6 months. At this time point we found that chronic exposure to the canola-rich diet resulted in a significant increase in body weight and impairments in their working memory together with decrease levels of post-synaptic density protein-95, a marker of synaptic integrity, and an increase in the ratio of insoluble Aβ 42/40. No significant changes were observed in tau phosphorylation and neuroinflammation. Taken together, our findings do not support a beneficial effect of chronic canola oil consumption on two important aspects of AD pathophysiology which includes memory impairments as well as synaptic integrity. While more studies are needed, our data do not justify the current trend aimed at replacing olive oil with canola oil.

Conflict of interest statement

The authors declare that they have no competing interests.

Figures

Figure 1
Figure 1
Chronic administration of canola oil-rich diet modulates behavioral responses of 3xTg mice. Six-month old 3xTg mice were randomized to receive regular chow diet (CTR) or diet enriched with canola oil (CO) until they were 12-month-old. (A) Mice were tested in the Y-maze paradigm for the number of entries, and the percentage of alternation. (B) Percentage of freezing in the contextual and cued phases of the fear conditioning paradigm. (C) Mice were also assessed in the Morris water maze paradigm for the number of entries to the platform zone, and the time spent in the platform zone. (CTR n = 11, CO, n = 10) (*p < 0.05).
Figure 2
Figure 2
Effect of chronic administration of canola oil-rich diet on brain Aβ levels and deposition. (A) RIPA-soluble (RIPA) and formic acid extractable (F.A.) Aβ 1-40 and Aβ 1-42 levels in brain cortex homogenates of 3xTg receiving vehicle (CTR) (n = 5) or canola oil (CO) (n = 5). (B) Ratios of Aβ 42/40 for RIPA soluble and formic acid soluble fraction measured in brain from 3xTg controls (CTR) or 3xTg treated with canola oil-rich diet (CO). (C) Quantification of the area occupied by Aβ immunoreactivity in brains of 3xTg mice receiving vehicle (CTR) (n = 3) or canola oil (CO) (n = 3). (D) Representative Western blots of APP, BACE1, ADAM10, APH1, Nicastrin, Pen2, PS1, ApoE, IDE and CD10 in the brain cortex homogenates from 3xTg mice receiving vehicle (CTR) (n = 4) or canola oil (CO) (n = 4). (E) Densitometric analyses of the immunoreactivities to the antibodies shown in the previous panel.
Figure 3
Figure 3
Effect of chronic administration of canola oil-rich diet on tau phosphorylation. (A) Representative Western blots of total soluble tau (HT7), phosphorylated tau at residues ser202/thr205 (AT8), thr231/ser235 (AT180), and thr181 (AT270) in brain cortex homogenates from 3xTg mice receiving vehicle (CTR) or canola oil for 6 months. (B) Densitometric analyses of the immunoreactivities to the antibodies shown in the previous panel (CO, n = 4; CTR, n = 4).
Figure 4
Figure 4
Effect of chronic administration of canola oil-rich diet on synaptic integrity and neuroinflammation. (A) Representative western blot analyses of synaptophysin (SYP) and post-synaptic density protein 95 (PSD95) in brain cortex homogenates of 3xTg mice treated with vehicle (CTR) or canola oil (CO). (B) Densitometric analyses of the immunoreactivities to the antibodies shown in the previous panel (CTR, n = 4; CO, n = 4) (*p < 0.05). (C) Representative images of brain sections from 3xTg mice receiving canola oil (CO) vehicle (CTR) immunostained with PSD95 antibody. (D) Representative western blot analyses of GFAP and IBA1 in brain cortex homogenates of 3xTg mice treated with vehicle (CTR) or canola oil (CO). (E) Densitometric analyses of the immunoreactivities to the antibodies shown in the previous panel (CTR, n = 4; CO, n = 4).
Figure 5
Figure 5
Effect of chronic administration of canola oil-rich diet on CREB signaling and autophagy. (A) Representative Western blot analyses of CREB pCREB, c-Fos, BDNF, in brain cortex homogenates of 3xTg mice receiving vehicle (CTR) or canola oil (CO) for 6 months. (B) Densitometric analyses of the immunoreactivities to the antibodies shown in the previous panel (CTR, n = 3, CO, n = 3). (C) Representative Western blot analyses of Atg5/12, Atg5, Atg7, LC3BI/II in brain cortex homogenates of 3xTg mice receiving vehicle (CTR) or canola oil (CO). (D) Densitometric analyses of the immunoreactivities to the antibodies shown in the previous panel (CTR, n = 4, CO, n = 4).

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