Abnormalities in kynurenine pathway metabolism in treatment-resistant depression and suicidality : a systematic review
(2017) In CNS and Neurological Disorders - Drug Targets 16(4). p.440-453- 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 neurobiological correlates of these complex conditions, their pathophysiology still remains unclear. Although the recent advances concerning the neurobiological determinants underlying 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... (More)
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 neurobiological correlates of these complex conditions, their pathophysiology still remains unclear. Although the recent advances concerning the neurobiological determinants underlying 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 at summarizing 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.
(Less)
- author
- organization
- publishing date
- 2017-04-13
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Kynurenine pathway, quinolinic acid, tryptophan, treatment-resistant depression, suicidal behavior
- in
- CNS and Neurological Disorders - Drug Targets
- volume
- 16
- issue
- 4
- pages
- 440 - 453
- publisher
- Bentham Science Publishers
- external identifiers
-
- scopus:85027269075
- wos:000405318900008
- pmid:28412922
- ISSN
- 1871-5273
- DOI
- 10.2174/1871527316666170413110605
- language
- English
- LU publication?
- yes
- id
- 22a9d1ac-a16c-4776-b17d-62d14812fab8
- date added to LUP
- 2017-04-30 15:04:34
- date last changed
- 2024-06-24 20:00:26
@article{22a9d1ac-a16c-4776-b17d-62d14812fab8,
abstract = {{<p>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 neurobiological correlates of these complex conditions, their pathophysiology still remains unclear. Although the recent advances concerning the neurobiological determinants underlying 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 at summarizing 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.</p>}},
author = {{Serafini, Gianluca and Adavastro, Giulia and Canepa, Giovanna and Capobianco, Laura and Conigliaro, Claudia and Pittaluga, Federica and Belvederi Murri, Martino and Valchera, Alessandro and De Berardis, Domenico and Pompili, Maurizio and Lindqvist, Daniel and Brundin, Lena and Amore, Mario}},
issn = {{1871-5273}},
keywords = {{Kynurenine pathway; quinolinic acid; tryptophan; treatment-resistant depression; suicidal behavior}},
language = {{eng}},
month = {{04}},
number = {{4}},
pages = {{440--453}},
publisher = {{Bentham Science Publishers}},
series = {{CNS and Neurological Disorders - Drug Targets}},
title = {{Abnormalities in kynurenine pathway metabolism in treatment-resistant depression and suicidality : a systematic review}},
url = {{http://dx.doi.org/10.2174/1871527316666170413110605}},
doi = {{10.2174/1871527316666170413110605}},
volume = {{16}},
year = {{2017}},
}