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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72 Citations

Opposing Control of Cannabinoid Receptor Stimulation on Amyloid-β-Induced Reactive Gliosis: In Vitro and in Vivo Evidence

The data support the assumption that compounds able to selectively block CB2 receptors may have therapeutic potential in controlling Aβ-related pathology, due to their beneficial effects devoid of psychotropic consequences.

CB2 cannabinoid receptor agonist ameliorates Alzheimer-like phenotype in AβPP/PS1 mice.

Support is lent to the idea that stimulation of CB2 receptors ameliorates several altered parameters in Alzheimer's disease such as impaired memory and learning, neuroinflammation, oxidative stress damage and oxidative stress responses, selected tau kinases, and tau hyperphosphorylation around plaques.

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

CB2 Cannabinoid Receptor As Potential Target against Alzheimer's Disease

Accumulated evidence suggests a role for CB2 receptors in Alzheimer's disease (AD) and indicates their potential as a therapeutic target against this neurodegenerative disease.

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.

S100B Inhibitor Pentamidine Attenuates Reactive Gliosis and Reduces Neuronal Loss in a Mouse Model of Alzheimer's Disease

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.

Knockdown of BACE1-AS Nonprotein-Coding Transcript Modulates Beta-Amyloid-Related Hippocampal Neurogenesis

A distortion of adult neurogenesis that is associated with Aβ production very early in amyloid pathogenesis is suggested and could prove useful as novel therapeutic targets and/or as early biomarkers of AD.
...

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