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The DOI matches its Crossref record; 69 of the 69 references it cites were found in a registry or an index.

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

Open access
Ramírez, Belén G., Blázquez, Cristina, del Pulgar, Teresa Gómez, Guzmán, Manuel, de Ceballos, María L.·2005·The Journal of Neuroscience

Abstract

Alzheimer's disease (AD) is characterized by enhanced β-amyloid peptide (βA) deposition along with glial activation in senile plaques, selective neuronal loss, and cognitive deficits. Cannabinoids are neuroprotective agents against excitotoxicity in vitro and acute brain damage in vivo. This background prompted us to study the localization, expression, and function of cannabinoid receptors in AD and the possible protective role of cannabinoids after βA treatment, both in vivo and in vitro. Here, we show that senile plaques in AD patients express cannabinoid receptors CB 1 and CB 2, together with markers of microglial activation, and that CB 1-positive neurons, present in high numbers in control cases, are greatly reduced in areas of microglial activation. In pharmacological experiments, we found that G-protein coupling and CB 1 receptor protein expression are markedly decreased in AD brains. Additionally, in AD brains, protein nitration is increased, and, more specifically, CB 1 and CB 2 proteins show enhanced nitration. Intracerebroventricular administration of the synthetic cannabinoid WIN55,212-2 to rats prevent βA-induced microglial activation, cognitive impairment, and loss of neuronal markers. Cannabinoids (HU-210, WIN55,212-2, and JWH-133) block βA-induced activation of cultured microglial cells, as judged by mitochondrial activity, cell morphology, and tumor necrosis factor-α release; these effects are independent of the antioxidant action of cannabinoid compounds and are also exerted by a CB 2-selective agonist. Moreover, cannabinoids abrogate microglia-mediated neurotoxicity after βA addition to rat cortical cocultures. Our results indicate that cannabinoid receptors are important in the pathology of AD and that cannabinoids succeed in preventing the neurodegenerative process occurring in the disease.

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Crossref · 10.1523/jneurosci.4540-04.2005

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Metadata

Authors
Ramírez, B. G., Blázquez, C., del Pulgar, T. G., Guzmán, M., & de Ceballos, M. L.
Venue
The Journal of Neuroscience
Published
2005-02-23
Volume
25
Issue
8
Pages
1904-1913
ISSN
  • 0270-6474 (ISSN-L)
  • 1529-2401
OpenAlex
W2028794471
Cited by
785
References
69
FWCI
24.09
Type
journal article
Language
en
Open access
hybrid

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CoChat. (2026). Citation check: Prevention of Alzheimer's Disease Pathology by Cannabinoids: Neuroprotection Mediated by Blockade of Microglial Activation. https://app.cochat.ai/papers/10.1523/jneurosci.4540-04.2005
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Ramírez, B. G., Blázquez, C., del Pulgar, T. G., Guzmán, M., & de Ceballos, M. L. (2005). Prevention of Alzheimer's Disease Pathology by Cannabinoids: Neuroprotection Mediated by Blockade of Microglial Activation. The Journal of Neuroscience. https://doi.org/10.1523/jneurosci.4540-04.2005

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.