Document Detail


Interferon-gamma-inducible kynurenines/pteridines inflammation cascade: implications for aging and aging-associated psychiatric and medical disorders.
MedLine Citation:
PMID:  20811799     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
This review of literature and our data suggests that up-regulated production of interferon-gamma (IFNG) in periphery and brain triggers a merger of tryptophan (TRY)-kynurenine (KYN) and guanine-tetrahydrobiopterin (BH4) metabolic pathways into inflammation cascade involved in aging and aging-associated medical and psychiatric disorders (AAMPD) (metabolic syndrome, depression, vascular cognitive impairment). IFNG-inducible KYN/pteridines inflammation cascade is characterized by up-regulation of nitric oxide synthase (NOS) activity (induced by KYN) and decreased formation of NOS cofactor, BH4, that results in uncoupling of NOS that shifting arginine from NO to superoxide anion production. Superoxide anion and free radicals among KYN derivatives trigger phospholipase A2-arachidonic acid cascade associated with AAMPD. IFNG-induced up-regulation of indoleamine 2,3-dioxygenase (IDO), rate-limiting enzyme of TRY-KYN pathway, decreases TRY conversion into serotonin (substrate of antidepressant effect) and increases production of KYN associated with diabetes [xanthurenic acid (XA)], anxiety (KYN), psychoses and cognitive impairment (kynurenic acid). IFNG-inducible KYN/pteridines inflammation cascade is impacted by IFNG (+874) T/A genotypes, encoding cytokine production. In addition to literature data on KYN/TRY ratio (IDO activity index), we observe neopterin levels (index of activity of rate-limiting enzyme of guanine-BH4 pathway) to be higher in carriers of high (T) than of low (A) producers alleles; and to correlate with AAMPD markers (e.g., insulin resistance, body mass index, mortality risk), and with IFN-alpha-induced depression in hepatitis C patients. IFNG-inducible cascade is influenced by environmental factors (e.g., vitamin B6 deficiency increases XA formation) and by pharmacological agents; and might offer new approaches for anti-aging and anti-AAMPD interventions.
Authors:
Gregory F Oxenkrug
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2010-09-02
Journal Detail:
Title:  Journal of neural transmission (Vienna, Austria : 1996)     Volume:  118     ISSN:  1435-1463     ISO Abbreviation:  J Neural Transm     Publication Date:  2011 Jan 
Date Detail:
Created Date:  2011-01-25     Completed Date:  2011-04-25     Revised Date:  2012-01-04    
Medline Journal Info:
Nlm Unique ID:  9702341     Medline TA:  J Neural Transm     Country:  Austria    
Other Details:
Languages:  eng     Pagination:  75-85     Citation Subset:  IM    
Affiliation:
Psychiatry and Inflammation Program, Department of Psychiatry, Tufts University/Tufts Medical Center, Boston, MA, USA. goxenkrug@tuftsmedicalcenter.org
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MeSH Terms
Descriptor/Qualifier:
Aging / genetics,  physiology*
Animals
Humans
Inflammation / genetics,  pathology*
Interferon-gamma / pharmacology*
Kynurenine / metabolism,  physiology*
Mental Disorders / genetics,  pathology*
Metabolic Syndrome X / genetics,  metabolism
Obesity / genetics,  pathology
Polymorphism, Genetic / genetics
Pteridines / metabolism*
Signal Transduction / drug effects
Grant Support
ID/Acronym/Agency:
MH083225/MH/NIMH NIH HHS; R21 MH083225-02/MH/NIMH NIH HHS
Chemical
Reg. No./Substance:
0/Pteridines; 343-65-7/Kynurenine; 82115-62-6/Interferon-gamma

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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