According to a new study, hemp extract containing cannabidiol (CBD) and cannabidiolic acid (CBDA) may help mitigate the cognitive impairments and brain inflammation associated with chronic stress.
Published in the Journal of Ethnopharmacology and conducted by researchers at Mae Fah Luang University, the study provides new insights into hemp’s potential neuroprotective properties.
The researchers explored the effects of CBD/CBDA-rich hemp extract on male Wistar rats subjected to chronic restraint stress (CRS), a widely used model for studying the impact of prolonged stress on the brain. Stress was induced by immobilizing the rats for six hours a day over 21 days.
According to the study’s abstract, “Hemp (Cannabis sativa L.) is increasingly being recognized for its medicinal properties,” and the plant’s high CBD content shows “promising neuroprotective properties without causing psychotomimetic or addictive effects.” However, the researchers noted that “the therapeutic potential of hemp extract remains inadequately explored,” particularly in addressing stress-induced cognitive impairment.
The study found that administering high doses of CBD/CBDA-rich hemp extract (10 and 30 mg/kg) one hour before restraint improved cognitive function in behavioral tests, including the Y-maze and object recognition tasks. Additionally, the extract reduced stress-related increases in corticosterone levels, adrenal gland weight, and hippocampal neuron damage.
“CBD/CBDA-rich hemp extract effectively ameliorated CRS-induced cognitive impairment and reversed HPA axis hyperactivity in CRS rats,” the researchers reported. The extract also decreased markers of glial activation, including microglial and astrocytic proteins, which are associated with inflammation and neurodegeneration.
Researchers conclude that “CBD/CBDA-rich hemp extracts remarkably reversed the stress-induced behavioral perturbations and hippocampal damage, suggesting its ameliorative effect on stress response.”
The study’s full abstract can be found below:
Abstract
Ethnopharmacological relevance: Hemp (Cannabis sativa L.) is increasingly being recognized for its medicinal properties beside utilizing it for food, oil, and textile fibers. The high level of cannabidiol (CBD) content in hemp’s flowers shows promising neuroprotective properties without causing psychotomimetic or addictive effects. Recently, products containing CBD and its precursor, cannabidiolic acid (CBDA), have been used to treat stress-related cognitive impairment. However, the therapeutic potential of hemp extract remains inadequately explored.
Aim of the study: To investigate the effect of CBD/CBDA-rich hemp extract on learning and memory, neuroendocrine alterations, and hippocampal neuropathological changes in the chronic restraint stress model.
Materials and methods: Chronic restraint stress (CRS) was induced in male Wistar rats by immobilizing them in a restrainer for 6 hours per day for 21 consecutive days. CBD/CBDA-rich hemp extract (10 and 30 mg/kg, intraperitoneal injection) was administered daily, 1 hour before restraint. After the last day of CRS, behavioral tests for cognition were conducted using the Y-maze and object recognition tests. Serum corticosterone (CORT) levels were measured by ELISA. Histopathological changes, neuronal density, and the activation of microglia and astrocytes were visualized using cresyl violet and immunohistochemical staining.
Results: A high dose of CBD/CBDA-rich hemp extract effectively ameliorated CRS-induced cognitive impairment and reversed HPA axis hyperactivity in CRS rats by reducing CORT levels and adrenal gland weight. Additionally, CBD/CBDA-rich hemp extract protected CRS-induced damage to hippocampal neurons. Further analysis showed that CBD/CBDA-rich hemp extract reduced specific markers of microglial activation (ionized calcium-binding adaptor molecule-1, Iba-1) and astrocytic structural protein (glial fibrillary acidic protein, GFAP) in CRS rats.
Conclusion: CBD/CBDA-rich hemp extracts remarkably reversed the stress-induced behavioral perturbations and hippocampal damage, suggesting its ameliorative effect on stress response.
