The genetic landscape of kynurenine predicts neurovascular pathology and disrupted white matter integrity in patients with mood disorders DOI
B. Bravi,

Lidia Fortanyer-Uyà,

Marco Paolini

и другие.

medRxiv (Cold Spring Harbor Laboratory), Год журнала: 2024, Номер unknown

Опубликована: Дек. 12, 2024

Abstract Low-grade systemic inflammation is linked to cardiometabolic diseases and increased cardiovascular risk. Patients with mood disorders, such as Major Depressive Disorder (MDD) Bipolar (BD), also show elevated risk inflammatory markers, suggesting shared biological pathways between conditions. The kynurenine (KYN) pathway, activated by cytokines involved in neurotransmitter systems mood, provides a promising area explore inflammatory-related genetic overlaps these increasing interest the SH2B3 rs3184504 SNP. Imaging markers like white matter hyperintensities (WMHs) (WM) microstructure alterations are associated disorders. This study aimed investigate load link KYN levels, polygenic score (PRS) its effect on (WMHs), outcomes of presumed vascular suffering, WM sample 95 MDD 80 BD patients. Higher PRS for was circulating levels KYN/TRP ratio. predicted presence WMHs. T variant higher number ratio were not WMHs, while positively correlated axial (AD) mean diffusivity (MD), nominal significance radial (RD). findings support contribution integrity indicates potential predisposition dysregulation, may modulate this

Язык: Английский

Redefining Roles: A Paradigm Shift in Tryptophan–Kynurenine Metabolism for Innovative Clinical Applications DOI Open Access
Masaru Tanaka,

Ágnes Szabó,

László Vécsei

и другие.

International Journal of Molecular Sciences, Год журнала: 2024, Номер 25(23), С. 12767 - 12767

Опубликована: Ноя. 27, 2024

The tryptophan-kynurenine (KYN) pathway has long been recognized for its essential role in generating metabolites that influence various physiological processes. Traditionally, these have categorized into distinct, often opposing groups, such as pro-oxidant versus antioxidant, excitotoxic/neurotoxic neuroprotective. This dichotomous framework shaped much of the research on conditions like neurodegenerative and neuropsychiatric disorders, well cancer, where metabolic imbalances are a key feature. effects significantly influenced by factors, including concentration particular cellular milieu which they generated. A molecule acts neuroprotective at low concentrations may exhibit neurotoxic elevated levels. oxidative equilibrium surrounding environment can alter function KYN from an antioxidant to pro-oxidant. narrative review offers comprehensive examination analysis contemporary understanding metabolites, emphasizing their multifaceted biological functions relevance numerous pathological underscores pressing necessity paradigm shift comprehension metabolism. Understanding context-dependent roles is vital novel therapies Alzheimer's disease, multiple sclerosis, cancer. Comprehensive modulation, balancing inflammatory signals enzyme regulation, promising avenues targeted, effective treatments.

Язык: Английский

Процитировано

4

UPF 648, a Selective KMO Inhibitor, Attenuates Psychomotor and Cognitive Impairment in Chronic Kidney Disease DOI
Aparajita Ghosh,

Neeraja Rayanki,

A. Joshi

и другие.

ACS Chemical Neuroscience, Год журнала: 2025, Номер 16(5), С. 908 - 919

Опубликована: Фев. 17, 2025

Kynurenine-3-monooxygenase (KMO), a key enzyme in the kynurenine pathway (KP) of tryptophan metabolism, converts into neurotoxic intermediate quinolinic acid (QA). QA, an N-methyl-d-aspartate (NMDA) receptor agonist, increases glutamate release and inhibits its reuptake, resulting excitotoxic cell death hippocampus striatum. Plasma metabolomics study exhibited KP metabolites as most altered patients with chronic kidney disease (CKD). Recently, QA was linked to kidney-brain axis one major neurotoxins responsible for cognitive impairment advanced CKD stages. Various preclinical models are being tested explore different intermediates that can be targeted ameliorate central nervous system (CNS) complications CKD. In this study, adenine-induced model developed C57BL/6 mice, where UPF 648, selective KMO inhibitor, administered observe changes hippocampus. Treatment 648 did not alter function or morphology inhibition led decreased plasma levels reduced pro-inflammatory cytokine interleukin-1-β (IL-1β). treatment ameliorated characteristic symptoms motor dysfunction, anxiety, depression, hippocampus-dependent memory. Important markers neuronal survival plasticity through brain-derived neurotrophic factor (BDNF)-tropomyosin kinase B (TRKB)-cAMP-responsive element binding protein 1 (CREB1) were upregulated after inhibition. conclusion, exciting target attenuate neuropsychiatric burden stages

Язык: Английский

Процитировано

0

Metabolic Syndrome and Schizophrenia: Adding a Piece to the Interplay Between the Kynurenine Pathway and Inflammation DOI Creative Commons
Jacopo Sapienza, Giulia Agostoni, Federica Repaci

и другие.

Metabolites, Год журнала: 2025, Номер 15(3), С. 176 - 176

Опубликована: Март 5, 2025

The biology of schizophrenia is highly complex and multifaceted. Numerous efforts have been made over the years to disentangle heterogeneity disease, gradually leading a more detailed understanding its underlying pathogenic mechanisms. Two cardinal elements in pathophysiology are neuroinflammation alterations neurotransmission. kynurenine (KYN) pathway (KP) particular importance because it inducted by systemic low-grade inflammation peripheral tissues, producing metabolites that neuroactive (i.e., modulating glutamatergic cholinergic neurotransmission), neuroprotective, or neurotoxic. Consequently, KP at crossroads between two primary systems involved pathogenesis schizophrenia. It bridges central nervous system (CNS) periphery, as can cross blood–brain barrier modulate neuronal activity. Metabolic syndrome plays crucial role this context, frequently co-occurs with schizophrenia, contributing sub-inflammatory state able activate KP. This narrative review provides valuable insights into these interactions, offering framework for developing targeted therapeutic interventions precision psychiatry approaches disorder.

Язык: Английский

Процитировано

0

Physiological and pathophysiological effects of L-tryptophan’s metabolites on the brain and immunity – a challenge for drug development DOI Creative Commons
Petar Iliev,

Samuil Ivanov,

S Lazarov

и другие.

Pharmacia, Год журнала: 2025, Номер 72, С. 1 - 7

Опубликована: Март 19, 2025

The dysregulation of the kynurenine branch from tryptophan (TRP) metabolism can cause an imbalance between neuroprotective kynurenic acid and neurotoxic metabolites in some psychiatric neurodegenerative disorders. Therefore, modulation TRP may contribute to novel therapeutic strategies for several neuropsychiatric diseases. Targeting L-TRP-kynurenine pathway enzymes, particularly involving indoleamine 2,3-dioxygenase-1, 2,3-dioxygenase, 3-monooxygenase, aminotransferase II, is a promising approach. future development potent selective inhibitors these enzymes with good safety profile would be potential new avenue treatment many essential amino L-Tryptophan, together its metabolites, plays key role diverse physiological pathophysiological processes brain, especially disorders autoimmunity. Also, vital biochemical precursor functional neuroactive molecules, including serotonin melatonin, which are great importance memory learning, emotional regulation, circadian cycle, hunger, pain, etc. This article aims underscore links tryptophan’s certain diseases central nervous system.

Язык: Английский

Процитировано

0

Kynurenine amplifies tetrahydrocannabinol-induced sensorimotor impairment and classic “tetrad” effects in mice DOI
Sabrine Bilel, Giorgia Corli,

Edoardo Tiziani

и другие.

Progress in Neuro-Psychopharmacology and Biological Psychiatry, Год журнала: 2025, Номер unknown, С. 111342 - 111342

Опубликована: Март 1, 2025

Язык: Английский

Процитировано

0

Kynurenine Pathway in Epilepsy: Unraveling Its Role in Glutamate Excitotoxicity, GABAergic Dysregulation, Neuroinflammation, and Mitochondrial Dysfunction DOI
Manpreet Kaur,

Pratyush Porel,

Ronak Y. Patel

и другие.

Neurotoxicity Research, Год журнала: 2025, Номер 43(2)

Опубликована: Март 28, 2025

Язык: Английский

Процитировано

0

Navigating Neurodegeneration: Integrating Biomarkers, Neuroinflammation, and Imaging in Parkinson’s, Alzheimer’s, and Motor Neuron Disorders DOI Creative Commons
Masaru Tanaka, Simone Battaglia, Donato Liloia

и другие.

Biomedicines, Год журнала: 2025, Номер 13(5), С. 1045 - 1045

Опубликована: Апрель 25, 2025

Neurodegenerative diseases represent a daunting global challenge, affecting millions worldwide and imposing significant clinical socioeconomic burdens [...]

Язык: Английский

Процитировано

0

Seventy-Five Years of Interactions: The Department of Physiology and Pharmacology at Karolinska Institutet andPharmacological Reviews DOI Open Access
Gunnar Schulte

Pharmacological Reviews, Год журнала: 2024, Номер 76(6), С. 972 - 977

Опубликована: Окт. 16, 2024

This special issue emerged from an informal discussion at editorial board meeting during 2023, where the 75th anniversaries of Pharmacological Reviews and Department Physiology Pharmacology Karolinska Institutet, Stockholm, Sweden were coincidentally discussed. The idea for

Язык: Английский

Процитировано

0

The genetic landscape of kynurenine predicts neurovascular pathology and disrupted white matter integrity in patients with mood disorders DOI
B. Bravi,

Lidia Fortanyer-Uyà,

Marco Paolini

и другие.

medRxiv (Cold Spring Harbor Laboratory), Год журнала: 2024, Номер unknown

Опубликована: Дек. 12, 2024

Abstract Low-grade systemic inflammation is linked to cardiometabolic diseases and increased cardiovascular risk. Patients with mood disorders, such as Major Depressive Disorder (MDD) Bipolar (BD), also show elevated risk inflammatory markers, suggesting shared biological pathways between conditions. The kynurenine (KYN) pathway, activated by cytokines involved in neurotransmitter systems mood, provides a promising area explore inflammatory-related genetic overlaps these increasing interest the SH2B3 rs3184504 SNP. Imaging markers like white matter hyperintensities (WMHs) (WM) microstructure alterations are associated disorders. This study aimed investigate load link KYN levels, polygenic score (PRS) its effect on (WMHs), outcomes of presumed vascular suffering, WM sample 95 MDD 80 BD patients. Higher PRS for was circulating levels KYN/TRP ratio. predicted presence WMHs. T variant higher number ratio were not WMHs, while positively correlated axial (AD) mean diffusivity (MD), nominal significance radial (RD). findings support contribution integrity indicates potential predisposition dysregulation, may modulate this

Язык: Английский

Процитировано

0