ArticleJournal of molecular neuroscience : MN2021
Orally Administered Cinnamon Extract Attenuates Cognitive and Neuronal Deficits Following Traumatic Brain Injury.
Article in Journal of molecular neuroscience : MN, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- A combination of Nrf-2 activator, kinetin and zinc provides neuroprotection through NLRP3-NF-ԟB signaling in traumatic brain injury.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Recent Advances on the Analysis and Biological Functions of Cinnamaldehyde and Its Derivatives.Antioxidants (Basel, Switzerland) · 2025Review
- Establishing a Mouse Model of NL3R617W-Associated Autism Spectrum Disorder for a Functional Study.Actas espanolas de psiquiatria · 2025Article
- Protective Effects of Plant-Derived Compounds Against Traumatic Brain Injury.Molecular neurobiology · 2024Review
- The effect ofSurgical neurology international · 2024Article
- Cognitive and Cellular Effects of Combined Organophosphate Toxicity and Mild Traumatic Brain Injury.Biomedicines · 2023Article
- Article
- Cinnamic Acid Attenuates Peripheral and Hypothalamic Inflammation in High-Fat Diet-Induced Obese Mice.Pharmaceutics · 2022Article
- Aqueous cinnamon extract ameliorates bowel dysfunction and enteric 5-HT synthesis in IBS rats.Frontiers in pharmacology · 2022Article
- Ketogenic Diet as a potential treatment for traumatic brain injury in mice.Scientific reports · 2021Article
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Authors and funding
5 authors.
Funding
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Abstract
The present paper shows how cinnamon extract (CE) consumption mitigates neuronal loss and memory impairment following traumatic brain injury (TBI), one of the world's most common neurodegenerative diseases. TBI patients suffer short- and long-term behavioral, cognitive, and emotional impairments, including difficulties in concentration, memory loss, and depression. Research shows that CE application can mitigate cognitive and behavioral impairments in animal models for Alzheimer's and Parkinson's disease, whose pathophysiology is similar to that of TBI. This study builds on prior research by showing similar results in TBI mice models. After drinking CE for a week, mice were injured using our 70-g weight drop TBI device. For 2 weeks thereafter, the mice continued drinking CE alongside standard lab nutrition. Subsequently, the mice underwent behavioral tests to assess their memory, motor activity, and anxiety. The mice brains were harvested for immunohistochemistry staining to evaluate overall neuronal survival. Our results show that CE consumption almost completely mitigates memory impairment and decreases neuronal loss after TBI. Mice that did not consume CE demonstrated impaired memory. Our results also show that CE consumption attenuated neuronal loss in the temporal cortex and the dentate gyrus. Mice that did not consume CE suffered a significant neuronal loss. There were no significant differences in anxiety levels and motor activity between all groups. These findings show a new therapeutic approach to improve cognitive function and decrease memory loss after TBI.
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