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Trans-Cinnamaldehyde Alleviates Amyloid-Beta Pathogenesis via the SIRT1-PGC1α-PPARγ Pathway in 5XFAD Transgenic Mice

1
Department of Biomedical Science and Technology, Graduate School, Kyung Hee University, 26 Kyungheedae-ro, Dongdaemun-gu, Seoul 02447, Korea
2
Department of Life and Nanopharmaceutical Sciences, Graduate School, Kyung Hee University, 26 Kyungheedae-ro, Dongdaemun-gu, Seoul 02447, Korea
3
Department of Fundamental Pharmaceutical Science, Graduate School, Kyung Hee University, 26 Kyungheedae-ro, Dongdaemun-gu, Seoul 02447, Korea
4
Department of Pharmaceutical Science, College of Pharmacy, Kyung Hee University, 26 Kyungheedae-ro, Dongdaemun-gu, Seoul 02447, Korea
5
Department of Oriental Pharmaceutical Science, College of Pharmacy, Kyung Hee University, 26 Kyungheedae-ro, Dongdaemun-gu, Seoul 02447, Korea
*
Authors to whom correspondence should be addressed.
The first two authors contributed equally to this work.
Int. J. Mol. Sci. 2020, 21(12), 4492; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21124492
Received: 6 June 2020 / Revised: 18 June 2020 / Accepted: 22 June 2020 / Published: 24 June 2020
(This article belongs to the Special Issue Regulatory Role of PPARs in the Disease)
Abnormal amyloid-β (Aβ) accumulation is the most significant feature of Alzheimer’s disease (AD). Among the several secretases involved in the generation of Aβ, β-secretase (BACE1) is the first rate-limiting enzyme in Aβ production that can be utilized to prevent the development of Aβ-related pathologies. Cinnamon extract, used in traditional medicine, was shown to inhibit the aggregation of tau protein and Aβ aggregation. However, the effect of trans-cinnamaldehyde (TCA), the main component of cinnamon, on Aβ deposition is unknown. Five-month-old 5XFAD mice were treated with TCA for eight weeks. Seven-month-old 5XFAD mice were evaluated for cognitive and spatial memory function. Brain samples collected at the conclusion of the treatment were assessed by immunofluorescence and biochemical analyses. Additional in vivo experiments were conducted to elucidate the mechanisms underlying the effect of TCA in the role of Aβ deposition. TCA treatment led to improvements in cognitive impairment and reduced Aβ deposition in the brains of 5XFAD mice. Interestingly, the levels of BACE1 were decreased, whereas the mRNA and protein levels of three well-known regulators of BACE1, silent information regulator 1 (SIRT1), peroxisome proliferator-activated receptor γ (PPARγ) coactivator 1α (PGC1α), and PPARγ, were increased in TCA-treated 5XFAD mice. TCA led to an improvement in AD pathology by reducing BACE1 levels through the activation of the SIRT1-PGC1α-PPARγ pathway, suggesting that TCA might be a useful therapeutic approach in AD. View Full-Text
Keywords: Alzheimer’s disease; amyloid-β; β-secretase; trans-cinnamaldehyde; SIRT1; PGC1α; PPARγ Alzheimer’s disease; amyloid-β; β-secretase; trans-cinnamaldehyde; SIRT1; PGC1α; PPARγ
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MDPI and ACS Style

Do, J.; Kim, N.; Jeon, S.H.; Gee, M.S.; Ju, Y.-J.; Kim, J.-H.; Oh, M.S.; Lee, J.K. Trans-Cinnamaldehyde Alleviates Amyloid-Beta Pathogenesis via the SIRT1-PGC1α-PPARγ Pathway in 5XFAD Transgenic Mice. Int. J. Mol. Sci. 2020, 21, 4492. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21124492

AMA Style

Do J, Kim N, Jeon SH, Gee MS, Ju Y-J, Kim J-H, Oh MS, Lee JK. Trans-Cinnamaldehyde Alleviates Amyloid-Beta Pathogenesis via the SIRT1-PGC1α-PPARγ Pathway in 5XFAD Transgenic Mice. International Journal of Molecular Sciences. 2020; 21(12):4492. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21124492

Chicago/Turabian Style

Do, Jimin, Namkwon Kim, Seung H. Jeon, Min S. Gee, Yeon-Joo Ju, Jong-Ho Kim, Myung S. Oh, and Jong K. Lee 2020. "Trans-Cinnamaldehyde Alleviates Amyloid-Beta Pathogenesis via the SIRT1-PGC1α-PPARγ Pathway in 5XFAD Transgenic Mice" International Journal of Molecular Sciences 21, no. 12: 4492. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21124492

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