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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http://dx.doi.org/10.1007/s12031-020-01688-4 | DOI Listing |
Sci Transl Med
January 2025
University of Strasbourg, INSERM, Strasbourg Translational Neuroscience & Psychiatry STEP-CRBS, UMR-S 1329, 67000 Strasbourg, France.
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January 2025
Department of Pharmaceutics, School of Pharmaceutical Education and Research, Jamia Hamdard, New Delhi, 110062, India.
The global prevalence of Parkinson's Disease (PD) is on the rise, driven by an ageing population and ongoing environmental conditions. To gain a better understanding of PD pathogenesis, it is essential to consider its relationship with the ageing process, as ageing stands out as the most significant risk factor for this neurodegenerative condition. PD risk factors encompass genetic predisposition, exposure to environmental toxins, and lifestyle influences, collectively increasing the chance of PD development.
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Huai'an Hospital Affiliated to Yangzhou University, The Fifth People's Hospital of Huai'an), 1 Huaihe East Road, Huaiyin District, Huai'an City, Jiangsu Province, China.
Ginkgolide B (GB) is a bioactive constituent found in Ginkgo biloba leaves that has been long recognized as a protective agent against many neurological disorders. Our study aimed to examine the effect of GB in an in vitro Parkinson's disease (PD) model and to investigate its neuroprotective mechanism as a primary objective. SK-N-SH cells were challenged with 1-methyl-4-phenylpyridinium (MPP) to act as a PD-like model of neuronal damage.
View Article and Find Full Text PDFNeuropsychiatr Dis Treat
January 2025
Department of Rehabilitation Medicine, The Affiliated Taian City Central Hospital of Qingdao University, Taian, 271000, People's Republic of China.
As the aging process accelerates and living conditions improve, central nervous system (CNS) diseases have become a major public health problem. Diseases of the CNS cause not only gray matter damage, which is primarily characterized by the loss of neurons, but also white matter damage. However, most previous studies have focused on grey matter injury (GMI), with fewer studies on white matter injury (WMI).
View Article and Find Full Text PDFUnilateral whisker denervation activates plasticity mechanisms and circuit adaptations in adults. Single nucleus RNA sequencing and multiplex fluorescence in situ hybridization revealed differentially expressed genes related to altered glutamate receptor distributions and synaptogenesis in thalamocortical (TC) recipient layer 4 (L4) neurons of the sensory cortex, specifically those receiving input from the intact whiskers after whisker denervation. Electrophysiology detected increased spontaneous excitatory events at L4 neurons, confirming an increase in synaptic connections.
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