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Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
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Inflammation-Associated Synaptic Alterations as Shared Threads in Depression and Multiple Sclerosis.

Antonio Bruno1, Ettore Dolcetti1, Francesca Romana Rizzo1

  • 1Synaptic Immunopathology Lab, Department of Systems Medicine, Tor Vergata University of Rome, Rome, Italy.

Frontiers in Cellular Neuroscience
|July 14, 2020
PubMed
Summary
This summary is machine-generated.

Inflammation plays a key role in Major Depressive Disorder (MDD) and Multiple Sclerosis (MS). This review explores how inflammation-induced synaptic changes in the brain contribute to depressive symptoms in both conditions.

Keywords:
antidepressant drugscytokinesexcitotoxicitymajor depressive disordermonoaminemultiple sclerosisneuroinflammationsynaptopathy

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Area of Science:

  • Neuroscience
  • Immunology
  • Psychiatry

Background:

  • Major Depressive Disorder (MDD) pathogenesis theories include monoamine and glutamate hypotheses.
  • Emerging evidence implicates inflammation and proinflammatory cytokines in mood disturbances and depression.
  • Chronic inflammatory diseases like Multiple Sclerosis (MS) are linked to a higher risk of MDD.

Purpose of the Study:

  • To review commonalities between MDD and MS.
  • To investigate inflammatory-dependent synaptic alterations in depression associated with both diseases.

Main Methods:

  • Review of existing literature on MDD, MS, and inflammation.
  • Analysis of studies examining synaptic function in the context of inflammation and depression.

Main Results:

  • Proinflammatory cytokines contribute to mood disturbances and depression.
  • Systemic inflammation can lead to anxiety, anhedonia, and fatigue.
  • Depressive symptoms in MS/EAE can manifest early, preceding disease onset.
  • Inflammatory-dependent synaptic dysfunctions occur in MS/EAE brains, independent of lesions.

Conclusions:

  • A complex interplay between immune and nervous systems impacts neurological functions, including depression.
  • Inflammation-induced synaptic alterations are a shared feature in MDD and MS.
  • Understanding these shared mechanisms may offer new therapeutic targets for depression.