the communication between the immune and nervous systems: the role of il-1β in synaptopathies

Clicks: 205
ID: 246800
2018
Free PDF
Article Quality & Performance Metrics
Overall Quality
Not rated
Combines reader engagement with the AI quality analysis. This article has not been analysed, so there is no overall score — reader engagement is measured and shown alongside.
AI Quality Assessment
Not analyzed
Readership in this journal
Steady

Ranked #178 of 189 articles by views in international journal of nanomedicine

Most read Least read

Bar heights use a square-root scale. Only the 120 most-read articles are drawn; the journal has 189 in total.

Mint this article as an NFT
Not yet minted

Create a permanent, verifiable on-chain record of this article on the Scimatic Network. The NFT is held in your Journament account, and you can withdraw it to your own wallet at any time.

5 SUSD one-off · no wallet required
Sign in to mint
Abstract
In the last 15 years, groundbreaking genetic progress has underlined a convergence onto coherent synaptic pathways for most psychiatric and neurodevelopmental disorders, which are now collectively called “synaptopathies.” However, the modest size of inheritance detected so far indicates a multifactorial etiology for these disorders, underlining the key contribution of environmental effects to them. Inflammation is known to influence the risk and/or severity of a variety of synaptopathies. In particular, pro-inflammatory cytokines, produced and released in the brain by activated astrocytes and microglia, may play a pivotal role in these pathologies. Although the link between immune system activation and defects in cognitive processes is nowadays clearly established, the knowledge of the molecular mechanisms by which inflammatory mediators specifically hit synaptic components implicated in synaptopathies is still in its infancy. This review summarizes recent evidence showing that the pro-inflammatory cytokine interleukin-1β (IL-1β) specifically targets synaptopathy molecular substrate, leading to memory defects and pathological processes. In particular, we describe three specific pathways through which IL-1β affects (1) synaptic maintenance/dendritic complexity, (2) spine morphology, and (3) the excitatory/inhibitory balance. We coin the term immune synaptopathies to identify this class of diseases.
Reference Key
pozzi2018frontiersthe Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Davide Pozzi, Elisabetta Menna, Alice Canzi, Genni Desiato, Cristina Mantovani, Michela Matteoli
Are you one of these authors? Claim your profile
Journal international journal of nanomedicine
Year 2018
DOI
10.3389/fnmol.2018.00111
URL
http://journal.frontiersin.org/article/10.3389/fnmol.2018.00111/full
Keywords
inflammation cytokines il-1β neuropsychiatry biological psychiatry

Citations

No citations found. To add a citation, contact the admin at info@scimatic.org

Comments

No comments yet. Be the first to comment on this article.