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FältnamnIndikatorerMetadata
00005422naa a2200493 4500
001oai:gup.ub.gu.se/287267
003SwePub
008240528s2019 | |||||||||||000 ||eng|
0247 a https://gup.ub.gu.se/publication/2872672 URI
0247 a https://doi.org/10.1186/s12974-019-1567-42 DOI
040 a (SwePub)gu
041 a eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
1001 a Chatterjee, Pratishtha4 aut
2451 0a Plasma neurofilament light chain and amyloid-β are associated with the kynurenine pathway metabolites in preclinical Alzheimer's disease.
264 c 2019-10-10
264 1b Springer Science and Business Media LLC,c 2019
520 a Blood markers indicative of neurodegeneration (neurofilament light chain; NFL), Alzheimer's disease amyloid pathology (amyloid-β; Aβ), and neuroinflammation (kynurenine pathway; KP metabolites) have been investigated independently in neurodegenerative diseases. However, the association of these markers of neurodegeneration and AD pathology with neuroinflammation has not been investigated previously. Therefore, the current study examined whether NFL and Aβ correlate with KP metabolites in elderly individuals to provide insight on the association between blood indicators of neurodegeneration and neuroinflammation.Correlations between KP metabolites, measured using liquid chromatography and gas chromatography coupled with mass spectrometry, and plasma NFL and Aβ concentrations, measured using single molecule array (Simoa) assays, were investigated in elderly individuals aged 65-90years, with normal global cognition (Mini-Mental State Examination Score≥26) from the Kerr Anglican Retirement Village Initiative in Ageing Health cohort.A positive correlation between NFL and the kynurenine to tryptophan ratio (K/T) reflecting indoleamine 2,3-dioxygenase activity was observed (r=.451, p<.0001). Positive correlations were also observed between NFL and kynurenine (r=.364, p<.0005), kynurenic acid (r=.384, p<.0001), 3-hydroxykynurenine (r=.246, p=.014), anthranilic acid (r=.311, p=.002), and quinolinic acid (r=.296, p=.003). Further, significant associations were observed between plasma Aβ40 and the K/T (r=.375, p<.0005), kynurenine (r=.374, p<.0005), kynurenic acid (r=.352, p<.0005), anthranilic acid (r=.381, p<.0005), and quinolinic acid (r=.352, p<.0005). Significant associations were also observed between plasma Aβ42 and the K/T ratio (r=.215, p=.034), kynurenic acid (r=.214, p=.035), anthranilic acid (r=.278, p=.006), and quinolinic acid (r=.224, p=.027) in the cohort. On stratifying participants based on their neocortical Aβ load (NAL) status, NFL correlated with KP metabolites irrespective of NAL status; however, associations between plasma Aβ and KP metabolites were only pronounced in individuals with high NAL while associations in individuals with low NAL were nearly absent.The current study shows that KP metabolite changes are associated with biomarker evidence of neurodegeneration. Additionally, the association between KP metabolites and plasma Aβ seems to be NAL status dependent. Finally, the current study suggests that an association between neurodegeneration and neuroinflammation manifests in the periphery, suggesting that preventing cytoskeleton cytotoxicity by KP metabolites may have therapeutic potential.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Medicinska och farmaceutiska grundvetenskaperx Neurovetenskaper0 (SwePub)301052 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Basic Medicinex Neurosciences0 (SwePub)301052 hsv//eng
7001 a Zetterberg, Henrik,d 1973u Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi,Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry4 aut0 (Swepub:gu)xzethe
7001 a Goozee, Kathryn4 aut
7001 a Lim, Chai K4 aut
7001 a Jacobs, Kelly R4 aut
7001 a Ashton, Nicholas J.u Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi,Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry4 aut0 (Swepub:gu)xashtn
7001 a Hye, Abdul4 aut
7001 a Pedrini, Steve4 aut
7001 a Sohrabi, Hamid R4 aut
7001 a Shah, Tejal4 aut
7001 a Asih, Prita R4 aut
7001 a Dave, Preeti4 aut
7001 a Shen, Kaikai4 aut
7001 a Taddei, Kevin4 aut
7001 a Lovejoy, David B4 aut
7001 a Guillemin, Gilles J4 aut
7001 a Blennow, Kaj,d 1958u Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi,Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry4 aut0 (Swepub:gu)xbleka
7001 a Martins, Ralph N4 aut
7102 a Göteborgs universitetb Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi4 org
7730 t Journal of neuroinflammationd : Springer Science and Business Media LLCg 16:1q 16:1x 1742-2094
8564 u https://jneuroinflammation.biomedcentral.com/track/pdf/10.1186/s12974-019-1567-4
8564 8u https://gup.ub.gu.se/publication/287267
8564 8u https://doi.org/10.1186/s12974-019-1567-4

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