The kynurenine pathway in major depressive disorder, bipolar disorder, and schizophrenia: a systematic review and meta-analysis of cerebrospinal fluid studies

Inam, Mehmet Enes; Fernandes, Brisa Simões; Salagre, Estela; Grande, Iría; Vieta, Eduard; Quevedo, Joao L De; Zhao, Zhongming

doi:10.47626/1516-4446-2022-2973

Cited by 1 publication

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“…For instance, a more recent review found that some features of BD, such as psychotic episodes and suicide attempts, may also be associated with an imbalance in kynurenine pathway metabolism, though this finding requires replication ( Bartoli et al, 2022 ). In addition, another recent meta-analysis of eight CSF studies found no evidence of increased KA levels or differences in TRP levels associated with BD ( Inam et al, 2023 ). Intriguingly, a recent study found that serum KYN levels were lower in BD patients than in healthy volunteers, but that hospitalized individuals with BD had lower KYN levels than stabilized outpatients; that study also found that longer duration of illness was associated with altered levels of TRP, KYN, QA, xanthurenic acid, and picolinic acid, suggesting that KYN pathway metabolites may serve as biomarkers related to acute symptomatology and longer duration of illness ( Skorobogatov et al, 2023 ).…”

Section: The Immune-inflammatory Systemmentioning

confidence: 99%

Non-canonical pathways in the pathophysiology and therapeutics of bipolar disorder

Machado-Vieira,

Courtes,

Zarate

et al. 2023

Front. Neurosci.

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Bipolar disorder (BD) is characterized by extreme mood swings ranging from manic/hypomanic to depressive episodes. The severity, duration, and frequency of these episodes can vary widely between individuals, significantly impacting quality of life. Individuals with BD spend almost half their lives experiencing mood symptoms, especially depression, as well as associated clinical dimensions such as anhedonia, fatigue, suicidality, anxiety, and neurovegetative symptoms. Persistent mood symptoms have been associated with premature mortality, accelerated aging, and elevated prevalence of treatment-resistant depression. Recent efforts have expanded our understanding of the neurobiology of BD and the downstream targets that may help track clinical outcomes and drug development. However, as a polygenic disorder, the neurobiology of BD is complex and involves biological changes in several organelles and downstream targets (pre-, post-, and extra-synaptic), including mitochondrial dysfunction, oxidative stress, altered monoaminergic and glutamatergic systems, lower neurotrophic factor levels, and changes in immune-inflammatory systems. The field has thus moved toward identifying more precise neurobiological targets that, in turn, may help develop personalized approaches and more reliable biomarkers for treatment prediction. Diverse pharmacological and non-pharmacological approaches targeting neurobiological pathways other than neurotransmission have also been tested in mood disorders. This article reviews different neurobiological targets and pathophysiological findings in non-canonical pathways in BD that may offer opportunities to support drug development and identify new, clinically relevant biological mechanisms. These include: neuroinflammation; mitochondrial function; calcium channels; oxidative stress; the glycogen synthase kinase-3 (GSK3) pathway; protein kinase C (PKC); brain-derived neurotrophic factor (BDNF); histone deacetylase (HDAC); and the purinergic signaling pathway.

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Section: The Immune-inflammatory Systemmentioning

confidence: 99%