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Emerging evidence suggests that the risk of developing chronic traumatic encephalopathy (CTE), a progressive neurodegenerative disease, is significantly increased in military personnel and contact sports players who have been exposed to repetitive trauma brain injury (TBI). Unfortunately there are no effective medications currently available for prevention and treatment of CTE.
Here we demonstrate that inhibition of monoacylglycerol lipase (MAGL), the key enzyme that metabolizes the endocannabinoid 2-arachidonoylglycerol (2-AG) in the brain, significantly reduced CTE-like neuropathologic changes in a mouse model of repetitive mild closed head injury (rmCHI). Inhibition of 2-AG metabolism promoted neurologic recovery following rmCHI and reduced proinflammatory cytokines, astroglial reactivity, expression of amyloid precursor protein and the enzymes that make Aβ, as well as formation of Aβ.
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Importantly, neurodegeneration, TDP-43 protein aggregation, and tau phosphorylation, which are the neuropathologic hallmarks of CTE, were significantly suppressed by MAGL inactivation. Furthermore, alterations in expression of glutamate receptor subunits and impairments in basal synaptic transmission, long-term synaptic plasticity, and spatial learning and memory were recovered by inhibition of 2-AG metabolism in animals exposed to rmCHI. Our results suggest that MAGL inhibition, which boosts 2-AG and reduces 2-AG metabolites prostaglandins in the brain, may lead to a new therapy for CTE. Monoacylglycerol lipase inhibition promotes neurologic recovery following repetitive mild closed head injury. ( A) Schematic illustration of the experimental protocol. Repetitive mild closed head injury (rmCHI) was induced using an electromagnetic controlled stereotaxic impact device. The black arrows represent the procedures (trauma brain injury (TBI) or sham), while the red arrows represent JZL184 injections.
Neurologic severity score (NSS), proinflammatory cytokines, astroglial reactivation, A β, the enzymes synthesizing A β, TDP-43 aggregation, tau phosphorylation, glutamate receptor subunits, basal synaptic transmission, long-term potentiation (LTP), and spatial learning and memory were detected using quantitative PCR (qPCR), western blot (WB), immunohistochemistry (IHC), electrophysiologic recordings, and the Morris water maze (MWM). ( B) Monoacylglycerol lipase inhibition improves neurologic recovery following rmTBI. JZL184 (10 mg/kg) or vehicle was injected intraperitoneally 30 minutes after each impact for 3 days.
NSS was assessed 2 hours after each TBI and 5 days after 3 impacts. The data are means±s.e.m. 
Neuroinflammation following repetitive mild closed head injury (rmCHI) is prevented by inhibition of monoacylglycerol lipase. ( A) Expression of proinflammatory markers vimentin (Vim) and cytokines, including interleukin (IL)-1 β, IL-6, and tumor necrosis factor alpha (TNF α).
Messenger RNA (mRNA) expression of cytokines in the ipsilateral brains from animals that received different treatments was analyzed using quantitative PCR 4 days after the first injury. The data are means±s.e.m.
Inhibition of 2-arachidonoylglycerol metabolism reduces traumatic brain injury-elevated formation of A β and expression of the enzymes that synthesize A β. ( A) Immunoblot analysis of amyloid precursor protein (APP), ADAM-10 ( α-secretase), BACE1 ( β-secretase), and nicastrin (NCT, a γ-secretase component) in the ipsilateral side of injured brains 8 days after the first TBI. The data are means±s.e.m. Transactive response DNA-binding protein (TDP) aggregation and tau phosphorylation after repetitive mild closed head injury are diminished by inhibition of 2-AG metabolism. ( A) Western blot analysis of brain cdk5, cdk5 regulatory subunits p25/p35, GSK3 β phosphorylation (p- GSK3 β), TDP-43, and tau phosphorylation (p-tau) 8 days after the first injury.
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Emerging evidence suggests that the risk of developing chronic traumatic encephalopathy (CTE), a progressive neurodegenerative disease, is significantly increased in military personnel and contact sports players who have been exposed to repetitive trauma brain injury (TBI). Unfortunately there are no effective medications currently available for prevention and treatment of CTE.
Here we demonstrate that inhibition of monoacylglycerol lipase (MAGL), the key enzyme that metabolizes the endocannabinoid 2-arachidonoylglycerol (2-AG) in the brain, significantly reduced CTE-like neuropathologic changes in a mouse model of repetitive mild closed head injury (rmCHI). Inhibition of 2-AG metabolism promoted neurologic recovery following rmCHI and reduced proinflammatory cytokines, astroglial reactivity, expression of amyloid precursor protein and the enzymes that make Aβ, as well as formation of Aβ.
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Importantly, neurodegeneration, TDP-43 protein aggregation, and tau phosphorylation, which are the neuropathologic hallmarks of CTE, were significantly suppressed by MAGL inactivation. Furthermore, alterations in expression of glutamate receptor subunits and impairments in basal synaptic transmission, long-term synaptic plasticity, and spatial learning and memory were recovered by inhibition of 2-AG metabolism in animals exposed to rmCHI. Our results suggest that MAGL inhibition, which boosts 2-AG and reduces 2-AG metabolites prostaglandins in the brain, may lead to a new therapy for CTE. Monoacylglycerol lipase inhibition promotes neurologic recovery following repetitive mild closed head injury. ( A) Schematic illustration of the experimental protocol. Repetitive mild closed head injury (rmCHI) was induced using an electromagnetic controlled stereotaxic impact device. The black arrows represent the procedures (trauma brain injury (TBI) or sham), while the red arrows represent JZL184 injections.
Neurologic severity score (NSS), proinflammatory cytokines, astroglial reactivation, A β, the enzymes synthesizing A β, TDP-43 aggregation, tau phosphorylation, glutamate receptor subunits, basal synaptic transmission, long-term potentiation (LTP), and spatial learning and memory were detected using quantitative PCR (qPCR), western blot (WB), immunohistochemistry (IHC), electrophysiologic recordings, and the Morris water maze (MWM). ( B) Monoacylglycerol lipase inhibition improves neurologic recovery following rmTBI. JZL184 (10 mg/kg) or vehicle was injected intraperitoneally 30 minutes after each impact for 3 days.
NSS was assessed 2 hours after each TBI and 5 days after 3 impacts. The data are means±s.e.m. Neuroinflammation following repetitive mild closed head injury (rmCHI) is prevented by inhibition of monoacylglycerol lipase. ( A) Expression of proinflammatory markers vimentin (Vim) and cytokines, including interleukin (IL)-1 β, IL-6, and tumor necrosis factor alpha (TNF α).
Messenger RNA (mRNA) expression of cytokines in the ipsilateral brains from animals that received different treatments was analyzed using quantitative PCR 4 days after the first injury. The data are means±s.e.m.
Inhibition of 2-arachidonoylglycerol metabolism reduces traumatic brain injury-elevated formation of A β and expression of the enzymes that synthesize A β. ( A) Immunoblot analysis of amyloid precursor protein (APP), ADAM-10 ( α-secretase), BACE1 ( β-secretase), and nicastrin (NCT, a γ-secretase component) in the ipsilateral side of injured brains 8 days after the first TBI. The data are means±s.e.m. Transactive response DNA-binding protein (TDP) aggregation and tau phosphorylation after repetitive mild closed head injury are diminished by inhibition of 2-AG metabolism. ( A) Western blot analysis of brain cdk5, cdk5 regulatory subunits p25/p35, GSK3 β phosphorylation (p- GSK3 β), TDP-43, and tau phosphorylation (p-tau) 8 days after the first injury.