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Cocaine mediated neuroinflammation: Role of dysregulated autophagy in pericytes - PMC
Source: ncbi.nlm.nih.gov
Article summary:
1. Cocaine exposure can induce inflammation in non-glial cells such as pericytes, which are important components of the neurovascular unit.
2. Cocaine exposure results in increased formation of autophagosomes and a concomitant defect in the fusion of the autophagosome with the lysosomes.
3. Pharmacological blocking of the sigma 1 receptor and interventions aimed at blocking either the sigma-1 receptor or the upstream ER stress mediators could likely be envisioned as promising therapeutic targets for abrogating cocaine-mediated inflammation in pericytes.
Article analysis:
The article is generally reliable and trustworthy, as it provides evidence from both in vitro and in vivo studies to support its claims. The authors have also provided a detailed discussion on their findings, which further adds to its credibility. However, there are some potential biases that should be noted. For example, the authors do not explore any counterarguments or alternative explanations for their findings, nor do they provide any evidence for potential risks associated with cocaine use or interventions aimed at blocking either the sigma-1 receptor or the upstream ER stress mediators. Additionally, while they discuss possible therapeutic targets for abrogating cocaine-mediated inflammation in pericytes, they do not provide any evidence to support these claims or explore any potential side effects associated with these interventions. Furthermore, while they discuss cocaine's effects on multiple cells of the CNS, they focus primarily on pericytes and do not provide an equal amount of detail regarding other cell types affected by cocaine exposure.