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内源性大麻素在神经退行性疾病中的作用研究进展
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Abstract:
神经退行性疾病(Neurodegenerative disease)是一类以神经元变性病变为基础的缓慢进展性疾病的总称，主要包括阿尔茨海默病(Alzheimer’s disease, AD)、帕金森病(Parkinson’s disease, PD)及肌萎缩侧索硬化症(amyotrophic lateral sclerosis, ALS)等。最近的研究发现内源性大麻素系统(endocannabinoid system, eCBs)可能是一种保护神经元免受伤害性刺激的内源性系统，对神经退行性疾病的病程有预防治疗作用。本文综述了eCBs对AD、PD及ALS的保护作用的几个方面，旨在为神经退行性疾病的治疗开辟新的策略和思路。
Neurodegenerative diseases are characterized by slowly progressive degeneration and/or death of nerve cells. Examples of neurodegenerative diseases contain Alzheimer’s disease (AD), Parkinson’s disease (PD) and amyotrophic lateral sclerosis (ALS). Recent studies reveal that endocannabinoid system may be an endogenous system that protects neurons from harmful stimuli and may have a preventive and therapeutic effect on the neurodegenerative diseases. Here we summarized several aspects of the eCBs protective effect of the AD, PD and ALS, aiming at providing promising thera-peutic targets and new strategy for neurodegenerative diseases.
| [1] | Ohno-Shosaku, T., Tanimura, A., Hashimotodani, Y., et al. (2012) Endocannabinoids and Retrograde Modulation of Synaptic Transmission. Neuroscientist, 18, 119-132. https://doi.org/10.1177/1073858410397377 |
| [2] | Xu, J. and Chen, C. (2015) Endocannabinoids in Synaptic Plasticity and Neuroprotection. Neuroscientist, 21, 152-168.
https://doi.org/10.1177/1073858414524632 |
| [3] | 朱时钰, 杨红卫. 大麻素2型受体在帕金森病中的神经保护作用研究进展[J]. 生命的化学, 2018, 38(4): 529-533. |
| [4] | Scotter, E.L., Abood, M.E. and Glass, M. (2010) The Endocannabinoid System as a Target for the Treatment of Neurodegenerative Disease. British Journal of Pharmacol-ogy, 160, 480-498.
https://doi.org/10.1111/j.1476-5381.2010.00735.x |
| [5] | Zhang, L., Wang, M., Bisogno, T., Di Marzo, V. and Alger, B.E. (2011) Endocannabinoids Generated by Ca2+or by Metabotropic Glutamate Receptors Appear to Arise from Different Pools of Diacylglycerol Lipase. PLoS ONE, 6, e16305.
https://doi.org/10.1371/journal.pone.0016305 |
| [6] | Raskin, J., Cummings, J., Hardy, J., Schuh, K. and Dean, R.A. (2015) Neurobiology of Alzheimer’s Disease: Integrated Molecular, Physiological, Anatomical, Biomarker, and Cognitive Dimensions. Current Alzheimer Research, 12, 712-722. https://doi.org/10.2174/1567205012666150701103107 |
| [7] | Chen, R., Zhang, J., Wu, Y., et al. (2012) Monoacylglycer-ol Lipase Is a Therapeutic Target for Alzheimer’s Disease. Cell Reports, 2, 1329-1339. https://doi.org/10.1016/j.celrep.2012.09.030 |
| [8] | Schm？le, A.C., Lundt, R., Toporowski, G., Hansen, J.N., et al. (2018) Cannabinoid Receptor 2-Deficiency AmelioratesDisease Symptoms in a Mouse Model with Alzheimer’s Dis-ease-Like Pathology. Journal of Alzheimer’s Disease, 64, 379-392. https://doi.org/10.3233/JAD-180230 |
| [9] | Gauthier, A., Vassiliou, G., Benoist, F., et al. (2003) Adipocyte Low Density Lipoprotein Receptor-Related Protein Gene Expression and Function Is Regulated by Peroxisome Prolifera-tor-Activated Receptor γ. Journal of Biological Chemistry, 278, 11945-11953. https://doi.org/10.1074/jbc.M212989200 |
| [10] | Tolón, R.M., Nú？ez, E., Pazos, M.R., et al. (2009) The Activation of Cannabinoid CB2 Receptors Stimulates in Situ and in Vitro Beta-Amyloid Removal by Human Macrophages. Brain Research, 1283, 148-154.
https://doi.org/10.1016/j.brainres.2009.05.098 |
| [11] | Chen, X., Zhang, J. and Chen, C. (2011) Endocanna-binoid 2-Arachidonoylglycerol Protects Neurons against β-Amyloid Insults. Neuroscience, 178, 159-168. https://doi.org/10.1016/j.neuroscience.2011.01.024 |
| [12] | Wu, J., Bie, B., Yang, H., et al. (2013) Activation of the CB2 Receptor System Reverses Amyloid-Induced Memory Deficiency. Neurobiology of Aging, 34, 791-804. https://doi.org/10.1016/j.neurobiolaging.2012.06.011 |
| [13] | Wolff, M.C. and Leander, J.D. (2003) SR141716A, a Cannabinoid CB1 Receptor Antagonist, Improves Memory in a Delayed Radial Maze Task. European Journal of Pharmacology, 477, 213-217.
https://doi.org/10.1016/j.ejphar.2003.08.025 |
| [14] | Martin-Moreno, A.M., Brera, B., Spuch, C., et al. (2012) Prolonged Oral Cannabinoid Administration Prevents Neuroinflammation, Lowers Beta-Amyloid Levels and Im-proves Cognitive Performance in Tg APP 2576 Mice. Neuroinflammation, 9, 8. https://doi.org/10.1186/1742-2094-9-8 |
| [15] | Ozaita, A., Puighermanal, E. and Maldonado, R. (2007) Regula-tion of PI3K/Akt/GSK-3 Pathway by Cannabinoids in the Brain. Journal of Neurochemistry, 102, 1105-1114. https://doi.org/10.1111/j.1471-4159.2007.04642.x |
| [16] | Giuffrida, A., Parsons, L.H., Kerr, T.M., et al. (1999) Dopa-mine Activation of Endogenous Cannabinoid Signaling in Dorsal Striatum. Nature Neuroscience, 2, 358-363. https://doi.org/10.1038/7268 |
| [17] | Marinelli, S, Di Marzo, V., Florenzano, F., Fezza, F., et al. (2007) N-Arachidonoyl-Dopamine Tunes Synaptic Transmission onto Dopaminergic Neurons by Activating Both Canna-binoid and Vanilloid Receptors. Neuropsychopharmacology, 32, 298-308. https://doi.org/10.1038/sj.npp.1301118 |
| [18] | 邹梓良, 查运红, 杨红卫. 内源性大麻素系统与帕金森病关系的研究进展[J]. 广东医学, 2015, 36(9): 1449-1451. |
| [19] | Kreitzer, A.C. and Malenka, R.C. (2005) Dopamine Modulation of State Dependent Endocannabinoid Release and Long-Term Depression in the Striatum. Neuroscience, 25, 10537-10545.
https://doi.org/10.1523/JNEUROSCI.2959-05.2005 |
| [20] | Venderova, K., Ruzicka, E., Vorisek, V. and Visnovsky, P. (2004) Survey on Cannabis Use in Parkinson’s Disease: Subjective Improvement of Motor Symptoms. Movement Disorders, 19, 1102-1106. https://doi.org/10.1002/mds.20111 |
| [21] | Wong, P., Pardo, C., Borchelt, D., et al. (1995) An Adverse Property of a Familial ALS-Linked SOD1 Mutation Causes Motor Neuron Disease Charac-terized by Vacuolar Degeneration of Mitochondria. Neuron, 14, 1105-1116.
https://doi.org/10.1016/0896-6273(95)90259-7 |
| [22] | Bruijn, L., Becher, M., Lee, M., et al. (1997) ALS-Linked SOD1 Mutant G85R Mediates Damage to Astro-Cytes and Promotes Rapidly Progressive Disease with SOD1-Containing Inclusions. Neuron, 18, 327-338.
https://doi.org/10.1016/S0896-6273(00)80272-X |
| [23] | Bilsland, L.G., Dick, J.R., Pryce, G., et al. (2006) In-creasing Cannabinoid Levels by Pharmacological and Genetic Manipulation Delay Disease Progression in SOD1 Mice. FASEB Journal, 29, 29. https://doi.org/10.1096/fj.05-4743fje |
| [24] | Kim, K., Moore, D.H., Makriyannis, A., et al. (2006) AM1241, a Cannabinoid CB2 Receptor Selective Compound, Delays Disease Pro-Gression in a Mouse Model of Amyotrophic Lateral Sclerosis. European Journal of Pharmacology, 542, 100-105. https://doi.org/10.1016/j.ejphar.2006.05.025 |
| [25] | Zhao, P., Ignacio, S., Beattie, E.C., et al. (2008) Altered Pre-symptom-Atic AMPA and Cannabinoid Receptor Trafficking in Motor Neurons of ALS Model Mice: Implications for Excitotoxicity. European Journal of Neuroscience, 27, 572-579. https://doi.org/10.1111/j.1460-9568.2008.06041.x |
| [26] | Rossi, S., De Chiara, V., Musella, A., et al. (2010) Abnormal Sensitivity of Cannabinoid CB1 Receptors in the Striatum of Mice with Experimental Amyotrophic Lateral Sclerosis. Amyotrophic Lateral Sclerosis, 19, 1-8.
https://doi.org/10.3109/17482960902977954 |
| [27] | Rothstein, J.D., Patel, S., Regan, M.R., et al. (2005) Be-ta-Lactam Antibiotics Offer Neuroprotection by Increasing Glutamate Transporter Expression. Nature, 433, 73-77. https://doi.org/10.1038/nature03180 |
