Objective: To investigate the effects of cannabidiol (CBD) on mitochondrial complex and creatine kinase (CK) activity in the rat brain using spectrophotometry.
Method: Male adult Wistar rats were given intraperitoneal injections of vehicle or CBD (15, 30, or 60 mg/kg) in an acute (single dose) or chronic (once daily for 14 consecutive days) regimen. The activities of mitochondrial complexes and CK were measured in the hippocampus, striatum, and prefrontal cortex.
Results: Both acute and chronic injection of CBD increased the activity of the mitochondrial complexes (I, II, II-III, and IV) and CK in the rat brain.
Conclusions: Considering that metabolism impairment is certainly involved in the pathophysiology of mood disorders, the modulation of energy metabolism (e.g., by increased mitochondrial complex and CK activity) by CBD could be an important mechanism implicated in the action of CBD.
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http://dx.doi.org/10.1590/1516-4446-2012-0886 | DOI Listing |
Background: Alzheimer's disease (AD) is a progressive neurodegenerative disease and the most prevalent type of senile dementia affecting more than 6 million Americans in 2023. Most of these AD cases are sporadic or late-onset AD with unclear etiology. Recent clinical trials on antibody drug clearing Ab plagues in brain show modest benefits of slowing down cognitive decline.
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December 2024
The University of Texas at San Antonio, San Antonio, TX, USA.
Background: Neurodegeneration is characterized by the progressive loss of neurons. However, the mechanisms by which neurons die in Alzheimer's disease (AD) remain elusive. Disrupted iron homeostasis is associated with accelerated cognitive decline, amyloid beta deposition, and AD progression, but its pathogenic relevance is poorly understood.
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December 2024
University of Pittsburgh School of Public Health, Pittsburgh, PA, USA.
Background: Many complex traits and diseases show sex-specific biases in clinical presentation and prevalence. For instance, two-thirds of AD cases are female. Studies suggest that women might have higher cognitive reserve but steeper cognitive decline in older age.
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December 2024
University Institute of Pharmaceutical sciences, Panjab University, Chandigarh, Chandigarh, India.
Background: Traumatic brain injury (TBI) due to external forces is a major cause of morbidity and mortality among people of all age groups, worldwide. Multiple biological processes like neuroinflammation, mitochondrial dysfunction, oxidative stress, amyloid β (Aβ) production, and tau hyperphosphorylation are involved in the pathogenesis of TBI. The role of neuroinflammation and oxidative stress has been suggested in the pathophysiology of brain injury-induced cognitive dysfunction.
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December 2024
University of Manitoba, Winnipeg, MB, Canada.
Background: Mitochondrial bioenergetics are essential for cellular function, specifically the intricacies of the electron transport chain (ETC), with Complex IV playing a crucial role in unraveling the mechanisms governing energy production. Mathematical models offer a valuable approach to simulate these complex processes, providing insights into normal mitochondrial function and aberrations associated with various diseases, including neurodegenerative disorders. Our research focuses on introducing and refining a mathematical model, emphasizing Complex IV in the ETC, with objectives including incorporating mitochondrial activity modulation using inhibiting and uncoupling reagents, akin to oxygen consumption experiments.
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