ReferenceID 4907
Trans-Cinnamaldehyde Alleviates Amyloid-Beta Pathogenesis via the SIRT1-PGC1α-PPARγ Pathway in 5XFAD Transgenic Mice
Int J Mol Sci
Abnormal amyloid-beta (Abeta) accumulation is the most significant feature of Alzheimer's disease (AD). Among the several secretases involved in the generation of Abeta, beta-secretase (BACE1) is the first rate-limiting
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- Reference Id
- 4907
- Evidence Id
- 21497
- Core Evidence Id
- 21497
- Source Reference Id
- 3078
- Herb2 Reference Id
- HBREF003875
- Subject Paper Key
- HBIN020653_32599846
- Pubmed Id
- 32599846
- Doi
- 10.3390/ijms21124492
- Paper Title
- Trans-Cinnamaldehyde Alleviates Amyloid-Beta Pathogenesis via the SIRT1-PGC1α-PPARγ Pathway in 5XFAD Transgenic Mice
- Paper Abstract
- Abnormal amyloid-beta (Abeta) accumulation is the most significant feature of Alzheimer's disease (AD). Among the several secretases involved in the generation of Abeta, beta-secretase (BACE1) is the first rate-limiting enzyme in Abeta production that can be utilized to prevent the development of Abeta-related pathologies. Cinnamon extract, used in traditional medicine, was shown to inhibit the aggregation of tau protein and Abeta aggregation. However, the effect of trans-cinnamaldehyde (TCA), the main component of cinnamon, on Abeta 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 Abeta deposition. TCA treatment led to improvements in cognitive impairment and reduced Abeta 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 gamma (PPARgamma) coactivator 1alpha (PGC1alpha), and PPARgamma, 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-PGC1alpha-PPARgamma pathway, suggesting that TCA might be a useful therapeutic approach in AD.
- Journal
- Int J Mol Sci
- Publish Year
- 2020
- Experiment Subject
- mouse
- Experiment Type
- Animal Experiment
- Phenotype Related
- Alzheimer's Disease; Cognitive Impairment; Abeta-related Pathologies
- Paper Title Cn
- Paper Title En
- Trans-Cinnamaldehyde Alleviates Amyloid-Beta Pathogenesis via the SIRT1-PGC1α-PPARγ Pathway in 5XFAD Transgenic Mice
- Bilingual Status
- semi_complete