CB1 receptor selective activation inhibits β-amyloid-induced iNOS protein expression in C6 cells and subsequently blunts tau protein hyperphosphorylation in co-cultured neurons

@article{Esposito2006CB1RS,
  title={CB1 receptor selective activation inhibits $\beta$-amyloid-induced iNOS protein expression in C6 cells and subsequently blunts tau protein hyperphosphorylation in co-cultured neurons},
  author={Giuseppe Esposito and Daniele De Filippis and Luca Steardo and Caterina Scuderi and Claudia Savani and Vincenzo Cuomo and Teresa Iuvone},
  journal={Neuroscience Letters},
  year={2006},
  volume={404},
  pages={342-346}
}
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71 Citations

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CB1 agonist ACEA protects neurons and reduces the cognitive impairment of AβPP/PS1 mice.

The present study shows that chronic administration of the cannabinoid receptor type 1 (CB1) receptor agonist arachidonyl-2-chloroethylamide (ACEA) at pre-symptomatic or at early symptomatic stages,…

The Acute Activation of the CB1 Receptor in the Hippocampus Decreases Neurotoxicity and Prevents Spatial Memory Impairment in Rats Lesioned with β-Amyloid 25–35

Gamma-linolenic acid ameliorates Aβ-induced neuroinflammation through NF-κB and MAPK signalling pathways

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Regulatory Role of Cannabinoid Receptor 1 in Stress-Induced Excitotoxicity and Neuroinflammation

Corresponding animal experiments indicated that a lack of CB1 produces hypothalamic/pituitary/adrenal (HPA) axis dysregulation and exacerbates stress-induced excitotoxic/neuroinflammatory responses, and multifaceted neuroprotective effects suggest that CB1 activation could be a new therapeutic strategy against neurological-neuropsychiatric pathologies with HPA axis Dysregulation and an excitOToxic/NEuroinflammatory component in their pathophysiology.

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It is demonstrated that pentamidine inhibits Aβ-induced gliosis and neuroinflammation in an animal model of AD, thus playing a role in slowing down the course of the disease.

Differential Cannabinoid Receptor Expression during Reactive Gliosis: a Possible Implication for a Nonpsychotropic Neuroprotection

The aim of this review is to clarify the function of the two cannabinoid receptors on glial cells and the differential role played by them, highlighting the emerging evidence of a CB2-mediated control of neuroinflammation that could liberate cannabinoids from the slavery of their central side effects.
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References

SHOWING 1-10 OF 27 REFERENCES

Cannabidiol inhibits inducible nitric oxide synthase protein expression and nitric oxide production in β-amyloid stimulated PC12 neurons through p38 MAP kinase and NF-κB involvement

Selective cannabinoid CB1 receptor‐mediated inhibition of inducible nitric oxide synthase protein expression in C6 rat glioma cells

The data suggest that selective cannabinoid CB1 receptor activation, by inhibiting iNOS expression and NO overproduction in glial cells, might be helpful in NO‐mediated inflammation leading to neurodegeneration.

The marijuana component cannabidiol inhibits β-amyloid-induced tau protein hyperphosphorylation through Wnt/β-catenin pathway rescue in PC12 cells

It is reported that cannabidiol inhibits hyperphosphorylation of tau protein in Aβ-stimulated PC12 neuronal cells, which is one of the most representative hallmarks in AD.

Astrocytic nitric oxide triggers tau hyperphosphorylation in hippocampal neurons.

It is found that the treatment of rat hippocampal astrocyte cultures with Abeta up-regulated the mRNA and protein levels of both the inducible and neuronal forms of nitric oxide synthase (iNOS and nNOS, respectively) and increased the production of Nitric oxide.

Prevention of Alzheimer's Disease Pathology by Cannabinoids: Neuroprotection Mediated by Blockade of Microglial Activation

It is shown that senile plaques in AD patients express cannabinoid receptors CB1 and CB2, together with markers of microglial activation, and that CB1-positive neurons, present in high numbers in control cases, are greatly reduced in areas of microgoo activation.

The Endocannabinoid System Protects Rat Glioma Cells Against HIV-1 Tat Protein-induced Cytotoxicity

The findings show that the endocannabinoid system, through the modulation of the l-arginine/NO pathway, reduces HIV-1 Tat-induced cytotoxicity, and is itself regulated by HIV- 1 Tat.

CB1 cannabinoid receptors are involved in neuroprotection via NF-κB inhibition

2-AG exerts its neuroprotection after CHI, at least in part, via CB1 receptor-mediated mechanisms that involve inhibition of intracellular inflammatory signaling pathways, which was as high as in the WT vehicle-treated mice.

Cannabinoid CB2 Receptors and Fatty Acid Amide Hydrolase Are Selectively Overexpressed in Neuritic Plaque-Associated Glia in Alzheimer's Disease Brains

Results show that both fatty acid amide hydrolase and cannabinoid CB2 receptors are abundantly and selectively expressed in neuritic plaque-associated astrocytes and microglia, respectively, whereas the expression of CB1 receptors remains unchanged.

Astrocytes down‐regulate neuronal β‐amyloid precursor protein expression and modify its processing in an apolipoprotein E isoform‐specific manner

It is concluded that astrocytes strongly regulate neuronal APP expression in primary neurons, and promote the amyloidogenic pathway in an apoE4‐dependent manner, which may modulate the pathogenesis of Alzheimer's disease.

Cannabinoid receptors and their role in neuroprotection

Two G protein-coupled receptors for marijuana’s psychoactive component, Δ9-tetrahydrocannabinol and CB1 and CB2 receptors, have been cloned to date and might represent an interesting target to develop neuroprotective agents.