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Current Medicinal Chemistry

Author(s): Laura Palagini*, Pierre Alexis Geoffroy and Dieter Riemann

DOI: 10.2174/0929867328666211214164907

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Sleep Markers in Psychiatry: Do Insomnia and Disturbed Sleep Play as Markers of Disrupted Neuroplasticity in Mood Disorders? A Proposed Model

Page: [5595 - 5605] Pages: 11

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Abstract

Introduction: Since insomnia and disturbed sleep may affect neuroplasticity, we aimed at reviewing their potential role as markers of disrupted neuroplasticity involved in mood disorders.

Methods: We performed a systematic review, according to PRIMA, on PubMed, PsycINFO and Embase electronic databases for literature regarding mood disorders, insomnia, sleep loss/deprivation in relation to different pathways involved in the impairment of neuroplasticity in mood disorders such as (1) alterations in neurodevelopment (2) activation of the stress system (3) neuroinflammation (4) neurodegeneration/neuroprogression, (5) deficit in neuroprotection.

Results: Sixty-five articles were analyzed and a narrative/ theoretical review was conducted. Studies showed that insomnia, sleep loss and sleep deprivation might impair brain plasticity of those areas involved in mood regulation throughout different pathways. Insomnia and disrupted sleep may act as neurobiological stressors by over-activating the stress and inflammatory systems, which may affect neural plasticity causing neuronal damage. In addition, disturbed sleep may favor a deficit in neuroprotection hence contributing to impaired neuroplasticity.

Conclusion: Insomnia and disturbed sleep may play a role as markers of alteration in brain plasticity in mood disorders. Assessing and targeting insomnia in the clinical practice may potentially play a neuroprotective role, contributing to “repairing” alterations in neuroplasticity or to the functional recovery of those areas involved in mood and emotion regulation.

Keywords: Insomnia, sleep loss, mood disorders, neuronal plasticity, sleep markers, neuroprogression, neuroinflammation, activation of stress system, oxidative stress, neuroprotection deficit.

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