Abstract
Neuroprotection by Cannabinoids in Neurodegenerative Diseases
Highlights
The recreational use of Cannabis Sativa preparations is known to most people [1]
CB1 and CB2 receptors share only 44% overall identity and 68% within the transmembrane domains. Both cannabinoid receptors are coupled to G proteins, mostly of the Gi/o type, through whose α subunit they inhibit the activity of adenylate cyclases and stimulate mitogenactivated protein kinases
This study showed that senile plaques in AD patients express CB1 and CB2 cannabinoid receptors as well as markers of microglial activation
Summary
The recreational use of Cannabis Sativa preparations is known to most people [1]. the medicinal use of Cannabis has a millenarian history that has been re-examined only very recently [2]. As early as 2600 BC, the Chinese emperor Huang Ti advised taking Cannabis for the relief of cramps and rheumatic and menstrual pain [3]. This long history of Cannabis medical use has resulted in the development of pharmaceutical drugs, such as Dronabinol and Cesamet. These preparations is based on ∆9-tetrahydrocannabinol (THC, Figure 1), which in 1964 was identified by Mechoulam and coworkers as the major psychoactive component of cannabis. Some 60 plant terpenophenols more or less related to THC have been isolated and defined cannabinoids [4]. ∆9-tetrahydrocannabinol, for its potency and abundance in cannabis, is the most important
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