The relationship between indoleamine 2,3-dioxygenase activity and post-stroke cognitive impairment

Gold, Allison; Herrmann, Nathan; Swardfager, Walter; Black, Sandra E.; Aviv, Richard I.; Tennen, Gayla; Kiss, Alexander; Lanctôt, Krista L.

doi:10.1186/1742-2094-8-17

Cited by 82 publications

(49 citation statements)

References 55 publications

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“…In fact, the L-Kyn/L-Trp ratio was able to identify subjects at risk of significant VCI. So far, this study is the only evidence which suggests a relationship between cognitive impairment and activation of the post-stroke kynurenine pathway [191]. However, it remains to be demonstrated whether a similar correlation between KP levels and VCI persists in the chronic phase of stroke and also which are the specific domains affected by the altered KP after stroke.…”

Section: Behavioral and Cognitive Effects Of Kynureninesmentioning

confidence: 77%

The Kynurenine Pathway in the Acute and Chronic Phases of Cerebral Ischemia

Cuartero

Parra²,

García‐Culebras³

et al. 2016

CPD

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Kynurenines are a wide range of catabolites which derive from tryptophan through the “Kynurenine Pathway” (KP). In addition to its peripheral role, increasing evidence shows a role of the KP in the central nervous system (CNS), mediating both physiological and pathological functions. Indeed, an imbalance in this route has been associated with several neurodegenerative disorders such as Alzheimer’s and Huntington’s diseases. Altered KP catabolism has also been described during both acute and chronic phases of stroke; however the contribution of the KP to the pathophysiology of acute ischemic damage and of post-stroke disorders during the chronic phase including depression and vascular dementia, and the exact mechanisms implicated in the regulation of the KP after stroke are not well established yet. A better understanding of the regulation and activity of the KP after stroke could provide new pharmacological tools in both acute and chronic phases of stroke. In this review, we will make an overview of CNS modulation by the KP. We will detail the KP contribution in the ischemic damage, how the unbalance of the KP might trigger an alteration of the cognitive function after stroke as well as potential targets for the development of new drugs.

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Section: Behavioral and Cognitive Effects Of Kynureninesmentioning

confidence: 77%

The Kynurenine Pathway in the Acute and Chronic Phases of Cerebral Ischemia

Cuartero

Parra²,

García‐Culebras³

et al. 2016

CPD

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“…By consuming tryptophan, IDO activation can therefore, in turn, reduce the synthesis of serotonin. Association of neuropsychiatric symptoms with increased kynurenine levels or altered kynurenine/tryptophan ratio has been demonstrated in several conditions associated with inflammation, including IFN-α-treated patients, aging, or Alzheimer's disease (Capuron et al, 2011c;Gulaj et al, 2010;Forrest et al, 2011;Gold et al, 2011;Raison et al, 2010). Microglial activation of the kynurenine pathway can also ultimately lead to the production of neuroactive glutamatergic compounds, including 3-hydroxykynurenine and quinolinic acid, which have a key role in neuronal death by stimulating NMDA receptors and promoting oxidative stress (Campbell et al, 2014;Dantzer and Walker, 2014;Stone et al, 2012).…”

Section: Neuropsychiatric Effects Of Inflammation: Evidence and Mechamentioning

confidence: 99%

Role of Adiposity-Driven Inflammation in Depressive Morbidity

Capuron

Lasselin

Castanon

2016

Neuropsychopharmacol

141

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Depression and metabolic disorders, including overweight and obesity, appear tightly interrelated. The prevalence of these conditions is concurrently growing worldwide, and both depression and overweight/obesity represent substantial risk factors for multiple medical complications. Moreover, there is now multiple evidence for a bidirectional relationship between depression and increased adiposity, with overweight/obesity being associated with an increased prevalence of depression, and in turn, depression augmenting the risk of weight gain and obesity. Although the reasons for this intricate link between depression and increased adiposity remain unclear, converging clinical and preclinical evidence points to a critical role for inflammatory processes and related alterations of brain functions. In support of this notion, increased adiposity leads to a chronic low-grade activation of inflammatory processes, which have been shown elsewhere to have a potent role in the pathophysiology of depression. It is therefore highly possible that adiposity-driven inflammation contributes to the development of depressive disorders and their growing prevalence worldwide. This review will present recent evidence in support of this hypothesis and will discuss the underlying mechanisms and potential therapeutic targets. Altogether, findings presented here should help to better understand the mechanisms linking adiposity to depression and facilitate the identification of new preventive and/or therapeutic strategies.

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“…In other clinical populations, elevated peripheral biomarkers of inflammation (CRP, IL-6) have been associated with neurocognitive decline such as delayed verbal learning tasks (Bettcher et al, 2012; Grassi-Oliveira et al, 2011; Hudetz et al, 2011) and impaired executive functioning (Hoshi et al, 2010; Mooijaart et al, 2013). Increased markers of indoleamine-2,3-dioxygenase activity in peripheral blood have been linked to poorer global cognitive performance in stroke survivors and cardiac patients following surgery (Forrest et al, 2011; Gold et al, 2011). Some of these effects may be hippocampus-dependent, as damage limited to the hippocampus has previously been associated with impaired recognition memory and verbal learning in patients suffering hypoxia-induced brain damage (Hopkins et al, 1995) and hippocampal impairments generally produce worse performance on NOR tests in rodent models, though this relationship continues to be explored (Antunes & Biala, 2012).…”

Section: Conclusion and Limitationsmentioning

confidence: 99%

Pre-treatment effects of peripheral tumors on brain and behavior: Neuroinflammatory mechanisms in humans and rodents

Schrepf¹,

Lutgendorf²,

Pyter³

2015

Brain, Behavior, and Immunity

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Cancer patients suffer high levels of affective and cognitive disturbances, which have been attributed to diagnosis-related distress, impairment of quality of life, and side effects of primary treatment. An inflammatory microenvironment is also a feature of the vast majority of solid tumors. However, the ability of tumor-associated biological processes to affect the central nervous system (CNS) has only recently been explored in the context of symptoms of depression and cognitive disturbances. In this review, we summarize the burgeoning evidence from rodent cancer models that solid tumors alter neurobiological pathways and subsequent behavioral processes with relevance to affective and cognitive disturbances reported in human cancer populations. We consider, in parallel, the evidence from human clinical cancer research demonstrating that affective and cognitive disturbances are common in some malignancies prior to diagnosis and treatment. We further consider the underlying neurobiological pathways, including altered neuroinflammation, tryptophan metabolism, prostaglandin synthesis and associated neuroanatomical changes, that are most strongly implicated in the rodent literature and supported by analogous evidence from human cancer populations. We focus on the implications of these findings for behavioral researchers and clinicians, with particular emphasis on methodological issues and areas of future research.

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The relationship between indoleamine 2,3-dioxygenase activity and post-stroke cognitive impairment

Cited by 82 publications

References 55 publications

The Kynurenine Pathway in the Acute and Chronic Phases of Cerebral Ischemia

The Kynurenine Pathway in the Acute and Chronic Phases of Cerebral Ischemia

Role of Adiposity-Driven Inflammation in Depressive Morbidity

Pre-treatment effects of peripheral tumors on brain and behavior: Neuroinflammatory mechanisms in humans and rodents

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