The Neuroprotective Effects of Cannabis-Derived Phytocannabinoids and Resveratrol in Parkinson’s Disease: A Systematic Review of Pre-clinical Studies

Prakash, Samay; Carter, Wayne G.

doi:10.20944/preprints202111.0050.v1

Cited by 9 publications

(1 citation statement)

References 74 publications

(279 reference statements)

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“…Neuroprotective properties of cannabinoids have also been suggested via elevated CB 2 expression in microglial cells within the substantia nigra of humans and animal models of PD [28]. A systematic review of Cannabis-derived phytocannabinoids in PD preclinical models demonstrated neuroprotective effects evidenced by increased dopamine levels and prolonged dopaminergic neuronal survival [29].…”

Section: Preclinical Evidencementioning

confidence: 99%

Advice to People with Parkinson’s in My Clinic: Cannabis

de Freitas,

Fox

2024

Journal of Parkinson’s Disease

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Cannabis (in all the varied methods of delivery) continues to garner significant attention as a potential therapeutic intervention for neurodegenerative disorders, including Parkinson’s disease (PD). The recent legalization of personal use of cannabis products in some parts of the world has increased this interest and with it, potential availability to many more people. However, such access has led to more questions than answers for both patients and health care professionals. These include what symptom(s) of PD will cannabis products treat; what dose; what type of cannabis product to use and what are the side effects?

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Section: Preclinical Evidencementioning

confidence: 99%

Advice to People with Parkinson’s in My Clinic: Cannabis

de Freitas,

Fox

2024

Journal of Parkinson’s Disease

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Alcohol Triggers the Accumulation of Oxidatively Damaged Proteins in Neuronal Cells and Tissues

Mudyanselage,

Wijamunige,

Kocoń

et al. 2024

Antioxidants

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Alcohol is toxic to neurons and can trigger alcohol-related brain damage, neuronal loss, and cognitive decline. Neuronal cells may be vulnerable to alcohol toxicity and damage from oxidative stress after differentiation. To consider this further, the toxicity of alcohol to undifferentiated SH-SY5Y cells was compared with that of cells that had been acutely differentiated. Cells were exposed to alcohol over a concentration range of 0–200 mM for up to 24 h and alcohol effects on cell viability were evaluated via MTT and LDH assays. Effects on mitochondrial morphology were examined via transmission electron microscopy, and mitochondrial functionality was examined using measurements of ATP and the production of reactive oxygen species (ROS). Alcohol reduced cell viability and depleted ATP levels in a concentration- and exposure duration-dependent manner, with undifferentiated cells more vulnerable to toxicity. Alcohol exposure resulted in neurite retraction, altered mitochondrial morphology, and increased the levels of ROS in proportion to alcohol concentration; these peaked after 3 and 6 h exposures and were significantly higher in differentiated cells. Protein carbonyl content (PCC) lagged behind ROS production and peaked after 12 and 24 h, increasing in proportion to alcohol concentration, with higher levels in differentiated cells. Carbonylated proteins were characterised by their denatured molecular weights and overlapped with those from adult post-mortem brain tissue, with levels of PCC higher in alcoholic subjects than matched controls. Hence, alcohol can potentially trigger cell and tissue damage from oxidative stress and the accumulation of oxidatively damaged proteins.

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An Investigation of the Neurotoxic Effects of Malathion, Chlorpyrifos, and Paraquat to Different Brain Regions

et al. 2022

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Acute or chronic exposures to pesticides have been linked to neurotoxicity and the potential development of neurodegenerative diseases (NDDs). This study aimed to consider the neurotoxicity of three widely utilized pesticides: malathion, chlorpyrifos, and paraquat within the hippocampus (HC), corpus striatum (CS), cerebellum (CER), and cerebral cortex (CC). Neurotoxicity was evaluated at relatively low, medium, and high pesticide dosages. All pesticides inhibited acetylcholinesterase (AChE) and neuropathy target esterase (NTE) in each of the brain regions, but esterase inhibition was greatest in the HC and CS. Each of the pesticides also induced greater disruption to cellular bioenergetics within the HC and CS, and this was monitored via inhibition of mitochondrial complex enzymes I and II, reduced ATP levels, and increased lactate production. Similarly, the HC and CS were more vulnerable to redox stress, with greater inhibition of the antioxidant enzymes catalase and superoxide dismutase and increased lipid peroxidation. All pesticides induced the production of nuclear Nrf2 in a dose-dependent manner. Collectively, these results show that pesticides disrupt cellular bioenergetics and that the HC and CS are more susceptible to pesticide effects than the CER and CC.

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The Neuroprotective Effects of Cannabis-Derived Phytocannabinoids and Resveratrol in Parkinson’s Disease: A Systematic Review of Pre-clinical Studies

Cited by 9 publications

References 74 publications

Advice to People with Parkinson’s in My Clinic: Cannabis

Advice to People with Parkinson’s in My Clinic: Cannabis

Alcohol Triggers the Accumulation of Oxidatively Damaged Proteins in Neuronal Cells and Tissues

An Investigation of the Neurotoxic Effects of Malathion, Chlorpyrifos, and Paraquat to Different Brain Regions

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