دورية أكاديمية
Potential Therapeutic Targets to Modulate the Endocannabinoid System in Alzheimer’s Disease
| العنوان: | Potential Therapeutic Targets to Modulate the Endocannabinoid System in Alzheimer’s Disease |
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| المؤلفون: | Hina Kanwal, Moris Sangineto, Martina Ciarnelli, Pasqualina Castaldo, Rosanna Villani, Antonino Davide Romano, Gaetano Serviddio, Tommaso Cassano |
| المصدر: | International Journal of Molecular Sciences, Vol 25, Iss 7, p 4050 (2024) |
| بيانات النشر: | MDPI AG, 2024. |
| سنة النشر: | 2024 |
| المجموعة: | LCC:Biology (General) LCC:Chemistry |
| مصطلحات موضوعية: | neurodegenerative diseases, Alzheimer’s disease, endocannabinoid system, fatty acid amide hydrolase (FAAH), monoacylglycerol (MAGL), cannabinoid receptors (CB1R, Biology (General), QH301-705.5, Chemistry, QD1-999 |
| الوصف: | Alzheimer’s disease (AD), the most common neurodegenerative disease (NDD), is characterized by chronic neuronal cell death through progressive loss of cognitive function. Amyloid beta (Aβ) deposition, neuroinflammation, oxidative stress, and hyperphosphorylated tau proteins are considered the hallmarks of AD pathology. Different therapeutic approaches approved by the Food and Drug Administration can only target a single altered pathway instead of various mechanisms that are involved in AD pathology, resulting in limited symptomatic relief and almost no effect in slowing down the disease progression. Growing evidence on modulating the components of the endocannabinoid system (ECS) proclaimed their neuroprotective effects by reducing neurochemical alterations and preventing cellular dysfunction. Recent studies on AD mouse models have reported that the inhibitors of the fatty acid amide hydrolase (FAAH) and monoacylglycerol (MAGL), hydrolytic enzymes for N-arachidonoyl ethanolamine (AEA) and 2-arachidonoylglycerol (2-AG), respectively, might be promising candidates as therapeutical intervention. The FAAH and MAGL inhibitors alone or in combination seem to produce neuroprotection by reversing cognitive deficits along with Aβ-induced neuroinflammation, oxidative responses, and neuronal death, delaying AD progression. Their exact signaling mechanisms need to be elucidated for understanding the brain intrinsic repair mechanism. The aim of this review was to shed light on physiology and pathophysiology of AD and to summarize the experimental data on neuroprotective roles of FAAH and MAGL inhibitors. In this review, we have also included CB1R and CB2R modulators with their diverse roles to modulate ECS mediated responses such as anti-nociceptive, anxiolytic, and anti-inflammatory actions in AD. Future research would provide the directions in understanding the molecular mechanisms and development of new therapeutic interventions for the treatment of AD. |
| نوع الوثيقة: | article |
| وصف الملف: | electronic resource |
| اللغة: | English |
| تدمد: | 1422-0067 1661-6596 |
| العلاقة: | https://www.mdpi.com/1422-0067/25/7/4050Test; https://doaj.org/toc/1661-6596Test; https://doaj.org/toc/1422-0067Test |
| DOI: | 10.3390/ijms25074050 |
| الوصول الحر: | https://doaj.org/article/44bbea6429af49329f275c4f2b496946Test |
| رقم الانضمام: | edsdoj.44bbea6429af49329f275c4f2b496946 |
| قاعدة البيانات: | Directory of Open Access Journals |
Full Text Finder | تدمد: | 14220067 16616596 |
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| DOI: | 10.3390/ijms25074050 |