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Biomedicines
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The Therapeutic Effects of Cannabinoids in Neurodegenerative Diseases
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The Therapeutic Effects of Cannabinoids in Neurodegenerative Diseases

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Drug Discovery, Development and Delivery".

Deadline for manuscript submissions: closed (10 June 2022) | Viewed by 7707

Special Issue Editor

Dr. Nathaniel Milton

E-Mail Website
Guest Editor
Centre for Biomedical Science Research, School of Clinical and Applied Sciences, Leeds Beckett University, City Campus, Leeds LS1 3HE, UK
Interests: Alzheimer’s disease; cannabinoid receptor; cannabis; endocannabinoid; Huntington’s disease; neuroprotection; peptide cannabinoids; Parkinson’s disease; Prion disease; Spinocerebellar ataxia

Special Issue Information

Dear Colleagues,

This Special Issue focuses on cannabinoids in the broadest sense and their therapeutic actions in both models and patient settings linked to neurodegenerative diseases. There are numerous neurodegenerative diseases, plus pathologies and symptoms associated with these that can potentially be treated by cannabinoids. As well as the obvious neuroprotection routes, there are also symptom relief treatments that have huge potential. The development of cannabinoids as therapies for neurodegenerative diseases is a rapidly expanding field. The lack of effective therapies for long-term control of many neurodegenerative disorders has led to a search for new ways to exploit chemicals that can easily cross the blood–brain barrier. Among the most exciting class of chemicals that readily cross the blood–brain barrier are cannabinoids. The presence of cannabinoid receptors combined with suggested neuroprotective actions mediated by actions at the neuronal cannabinoid receptors has made this area a hot bed of development covered in this Special Issue. The plethora of symptoms associated with neurodegenerative diseases and the use of cannabinoids to relieve these symptoms is another up-and-coming area that will be covered.

 

Therefore, I am taking the liberty to invite all authors from the cannabinoid and neurodegenerative disease fields to contribute. Review and research articles that summarize and investigate the therapeutic role of cannabinoids in processes underlying the pathology of neurodegenerative disease, plus associated symptomatic changes are very welcome. Treatments that modify the endogenous cannabinoid system are another area in which papers are sought. In particular, the Special Issue aims to translate the results of basic research into the treatment of various neurodegenerative diseases. Articles demonstrating the potential of cannabinoids in neurodegenerative disorders not previously linked with cannabinoid therapy are particularly welcome alongside articles suggesting potential of novel cannabinoids.


Dr. Nathaniel Milton
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Alzheimer’s disease
  • cannabinoid receptor
  • cannabis
  • endocannabinoid
  • Huntington’s disease
  • neuroprotection
  • peptide cannabinoids
  • Parkinson’s disease
  • Prion disease
  • Spinocerebellar ataxia

Published Papers (2 papers)

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Research

22 pages, 4163 KiB  
Article
WIN55,212-2 Attenuates Cognitive Impairments in AlCl3 + d-Galactose-Induced Alzheimer’s Disease Rats by Enhancing Neurogenesis and Reversing Oxidative Stress
by Onesimus Mahdi, Samaila Musa Chiroma, Mohamad Taufik Hidayat Baharuldin, Nurul Huda Mohd Nor, Che Norma Mat Taib, Saravanan Jagadeesan, Shamala Devi and Mohamad Aris Mohd Moklas
Biomedicines 2021, 9(9), 1270; https://doi.org/10.3390/biomedicines9091270 - 19 Sep 2021
Cited by 13 | Viewed by 4073
Abstract
Neurotransmission and cognitive dysfunctions have been linked to old age disorders including Alzheimer’s disease (AD). Aluminium is a known neurotoxic metal, whereas d-galactose (d-gal) has been established as a senescence agent. WIN55,212-2 (WIN), is a potent cannabinoid agonist which partially [...] Read more.
Neurotransmission and cognitive dysfunctions have been linked to old age disorders including Alzheimer’s disease (AD). Aluminium is a known neurotoxic metal, whereas d-galactose (d-gal) has been established as a senescence agent. WIN55,212-2 (WIN), is a potent cannabinoid agonist which partially restores neurogenesis in aged rats. The current study aimed to explore the therapeutic potentials of WIN on Aluminium chloride (AlCl3) and d-gal-induced rat models with cognitive dysfunction. Healthy male albino Wistar rats weighing between 200–250 g were injected with d-gal 60 mg/kg intra peritoneally (i.p), while AlCl3 (200 mg/kg) was orally administered once daily for 10 consecutive weeks. Subsequently, from weeks 8–11 rats were co-administered with WIN (0.5, 1 and 2 mg/kg/day) and donepezil 1 mg/kg. The cognitive functions of the rats were assessed with a Morris water maze (MWM). Furthermore, oxidative stress biomarkers; malondialdehyde (MDA), superoxide dismutase (SOD), glutathione (GSH) and neurogenesis markers: Nestin and glial fibrillary acidic protein (GFAP) were also evaluated, as well as the histology of the hippocampus. The results revealed that rats exposed to AlCl3 and d-gal alone showed cognitive impairments and marked neuronal loss (p < 0.05) in their hippocampal conus ammonis 1 (CA1). Additionally, a significant decrease in the expressions of GFAP and Nestin was also observed, including increased levels of MDA and decreased levels of SOD and GSH. However, administration of WIN irrespective of the doses given reversed the cognitive impairments and the associated biochemical derangements. As there were increases in the levels SOD, GSH, Nestin and GFAP (p < 0.05), while a significant decrease in the levels of MDA was observed, besides attenuation of the aberrant cytoarchitecture of the rat’s hippocampi. The biochemical profiles of the WIN-treated rats were normal. Thus, these findings offer possible scientific evidence of WIN being an effective candidate in the treatment of AD-related cognitive deficits. Full article
(This article belongs to the Special Issue The Therapeutic Effects of Cannabinoids in Neurodegenerative Diseases)
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15 pages, 2708 KiB  
Article
WIN55,212-2, a Dual Modulator of Cannabinoid Receptors and G Protein-Coupled Inward Rectifier Potassium Channels
by Dongchen An, Steve Peigneur and Jan Tytgat
Biomedicines 2021, 9(5), 484; https://doi.org/10.3390/biomedicines9050484 - 28 Apr 2021
Cited by 3 | Viewed by 2835
Abstract
The coupling of cannabinoid receptors, CB1 and CB2, to G protein-coupled inward rectifier potassium channels, GIRK1 and GIRK2, modulates neuronal excitability in the human brain. The present study established and validated the functional expression in a Xenopus laevis oocyte expression system of CB1 [...] Read more.
The coupling of cannabinoid receptors, CB1 and CB2, to G protein-coupled inward rectifier potassium channels, GIRK1 and GIRK2, modulates neuronal excitability in the human brain. The present study established and validated the functional expression in a Xenopus laevis oocyte expression system of CB1 and CB2 receptors, interacting with heteromeric GIRK1/2 channels and a regulator of G protein signaling, RGS4. This ex vivo system enables the discovery of a wide range of ligands interacting orthosterically or allosterically with CB1 and/or CB2 receptors. WIN55,212-2, a non-selective agonist of CB1 and CB2, was used to explore the CB1- or CB2-GIRK1/2-RGS4 signaling cascade. We show that WIN55,212-2 activates CB1 and CB2 at low concentrations whereas at higher concentrations it exerts a direct block of GIRK1/2. This illustrates a dual modulatory function, a feature not described before, which helps to explain the adverse effects induced by WIN55,212-2 in vivo. When comparing the effects with other typical cannabinoids such as Δ9-THC, CBD, CP55,940, and rimonabant, only WIN55,212-2 can significantly block GIRK1/2. Interestingly, the inward rectifier potassium channel, IRK1, a non-G protein-coupled potassium channel important for setting the resting membrane voltage and highly similar to GIRK1 and GIRK2, is not sensitive to WIN55,212-2, Δ9-THC, CBD, CP55,940, or rimonabant. From this, it is concluded that WIN55,212-2 selectively blocks GIRK1/2. Full article
(This article belongs to the Special Issue The Therapeutic Effects of Cannabinoids in Neurodegenerative Diseases)
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