Treatment resistant depression (TRD) and suicidal behavior are among the most important public health problems and are commonly associated with significant disability and psychosocial impairment. Although there have been recent advances in identifying the neurobiological correlates of these complex conditions, their pathophysiology still remains unclear. Compared to non-suicidal subjects, higher mean concentrations of inflammatory mediators have been found in both the periphery and brain of individuals at risk for suicide. Several lines of evidence suggest that neuroinflammation is accompanied by a dysregulation of the kynurenine pathway (KP) in both TRD and suicidal individuals, resulting in an imbalance of neuroactive metabolites. In particular, neuroinflammation may trigger an increased production of the N-Methyl-D-aspartate (NMDA) receptor agonist quinolinic acid and a concomitant reduction of neuroprotective metabolites, potentially causing downstream effects in glutamatergic systems resulting in depressive symptoms and suicidal behavior. This systematic review of the current literature is mainly aimed to summarize the most important evidence pertaining to KP metabolism abnormalities in TRD and suicidal behavior. Targeting the KP enzymes may provide innovative approaches in the management of both TRD and suicidality

Abnormalities in kynurenine pathway metabolism in treatment-resistant depression and suicidality: a systematic review / Serafini, Gianluca; Adavastro, Giulia; Canepa, Giovanna; Capobianco, Laura; Conigliaro, Claudia; Pittaluga, Federica; Murri, Martino Belvederi; Valchera, Alessandro; De Berardis, Domenico; Pompili, Maurizio; Lindqvist, Daniel; Brundin, Lena; Amore, Mario. - In: CNS & NEUROLOGICAL DISORDERS. DRUG TARGETS. - ISSN 1871-5273. - 16:4(2017), pp. 440-453. [10.2174/1871527316666170413110605]

Abnormalities in kynurenine pathway metabolism in treatment-resistant depression and suicidality: a systematic review

Pompili, Maurizio;Amore, Mario
2017

Abstract

Treatment resistant depression (TRD) and suicidal behavior are among the most important public health problems and are commonly associated with significant disability and psychosocial impairment. Although there have been recent advances in identifying the neurobiological correlates of these complex conditions, their pathophysiology still remains unclear. Compared to non-suicidal subjects, higher mean concentrations of inflammatory mediators have been found in both the periphery and brain of individuals at risk for suicide. Several lines of evidence suggest that neuroinflammation is accompanied by a dysregulation of the kynurenine pathway (KP) in both TRD and suicidal individuals, resulting in an imbalance of neuroactive metabolites. In particular, neuroinflammation may trigger an increased production of the N-Methyl-D-aspartate (NMDA) receptor agonist quinolinic acid and a concomitant reduction of neuroprotective metabolites, potentially causing downstream effects in glutamatergic systems resulting in depressive symptoms and suicidal behavior. This systematic review of the current literature is mainly aimed to summarize the most important evidence pertaining to KP metabolism abnormalities in TRD and suicidal behavior. Targeting the KP enzymes may provide innovative approaches in the management of both TRD and suicidality
2017
kynurenine pathway; metabolism; quinolinic acid; suicidal behavior; treatment resistant depression; tryptophan; neuroscience; pharmacology
01 Pubblicazione su rivista::01a Articolo in rivista
Abnormalities in kynurenine pathway metabolism in treatment-resistant depression and suicidality: a systematic review / Serafini, Gianluca; Adavastro, Giulia; Canepa, Giovanna; Capobianco, Laura; Conigliaro, Claudia; Pittaluga, Federica; Murri, Martino Belvederi; Valchera, Alessandro; De Berardis, Domenico; Pompili, Maurizio; Lindqvist, Daniel; Brundin, Lena; Amore, Mario. - In: CNS & NEUROLOGICAL DISORDERS. DRUG TARGETS. - ISSN 1871-5273. - 16:4(2017), pp. 440-453. [10.2174/1871527316666170413110605]
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11573/1044438
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