Abstract
Amyotrophic Lateral Sclerosis (ALS) currently lacks a robust and well-defined biomarker that can 1) assess the progression of the disease, 2) predict and/or delineate the various clinical subtypes, and 3) evaluate or predict a patient’s response to treatments. The kynurenine Pathway (KP) of tryptophan degradation represent a promising candidate as it is involved with several neuropathological features present in ALS including neuroinflammation, excitotoxicity, oxidative stress, immune system activation and dysregulation of energy metabolism. Some of the KP metabolites (KPMs) can cross the blood brain barrier, and many studies have shown their levels are dysregulated in major neurodegenerative diseases including ALS. The KPMs can be easily analyzed in body fluids and tissue and as they are small molecules, and are stable. KPMs have a Janus face action, they can be either or both neurotoxic and/or neuroprotective depending of their levels. This mini review examines and presents evidence supporting the use of KPMs as a relevant set of biomarkers for ALS, and highlights the criteria required to achieve a valid biomarker set for ALS.
| Language | English |
|---|---|
| Article number | 1013 |
| Pages | 1-11 |
| Number of pages | 11 |
| Journal | Frontiers in Neuroscience |
| Volume | 13 |
| DOIs | |
| Publication status | Published - 20 Sep 2019 |
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Bibliographical note
Copyright the Author(s) 2019. Version archived for private and non-commercial use with the permission of the author/s and according to publisher conditions. For further rights please contact the publisher.Keywords
- amyotrophic lateral sclerosis
- biomarker development
- kynurenine pathway
- motor neuron disease
- neurodegeneration
- neuroinflammation and neurodegeneration
- tryptophan
Cite this
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Kynurenine pathway metabolites as biomarkers for Amyotrophic Lateral Sclerosis. / Tan, Vanessa X.; Guillemin, Gilles J.
In: Frontiers in Neuroscience, Vol. 13, 1013, 20.09.2019, p. 1-11.Research output: Contribution to journal › Review article › Research › peer-review
TY - JOUR
T1 - Kynurenine pathway metabolites as biomarkers for Amyotrophic Lateral Sclerosis
AU - Tan, Vanessa X.
AU - Guillemin, Gilles J.
N1 - Copyright the Author(s) 2019. Version archived for private and non-commercial use with the permission of the author/s and according to publisher conditions. For further rights please contact the publisher.
PY - 2019/9/20
Y1 - 2019/9/20
N2 - Amyotrophic Lateral Sclerosis (ALS) currently lacks a robust and well-defined biomarker that can 1) assess the progression of the disease, 2) predict and/or delineate the various clinical subtypes, and 3) evaluate or predict a patient’s response to treatments. The kynurenine Pathway (KP) of tryptophan degradation represent a promising candidate as it is involved with several neuropathological features present in ALS including neuroinflammation, excitotoxicity, oxidative stress, immune system activation and dysregulation of energy metabolism. Some of the KP metabolites (KPMs) can cross the blood brain barrier, and many studies have shown their levels are dysregulated in major neurodegenerative diseases including ALS. The KPMs can be easily analyzed in body fluids and tissue and as they are small molecules, and are stable. KPMs have a Janus face action, they can be either or both neurotoxic and/or neuroprotective depending of their levels. This mini review examines and presents evidence supporting the use of KPMs as a relevant set of biomarkers for ALS, and highlights the criteria required to achieve a valid biomarker set for ALS.
AB - Amyotrophic Lateral Sclerosis (ALS) currently lacks a robust and well-defined biomarker that can 1) assess the progression of the disease, 2) predict and/or delineate the various clinical subtypes, and 3) evaluate or predict a patient’s response to treatments. The kynurenine Pathway (KP) of tryptophan degradation represent a promising candidate as it is involved with several neuropathological features present in ALS including neuroinflammation, excitotoxicity, oxidative stress, immune system activation and dysregulation of energy metabolism. Some of the KP metabolites (KPMs) can cross the blood brain barrier, and many studies have shown their levels are dysregulated in major neurodegenerative diseases including ALS. The KPMs can be easily analyzed in body fluids and tissue and as they are small molecules, and are stable. KPMs have a Janus face action, they can be either or both neurotoxic and/or neuroprotective depending of their levels. This mini review examines and presents evidence supporting the use of KPMs as a relevant set of biomarkers for ALS, and highlights the criteria required to achieve a valid biomarker set for ALS.
KW - amyotrophic lateral sclerosis
KW - biomarker development
KW - kynurenine pathway
KW - motor neuron disease
KW - neurodegeneration
KW - neuroinflammation and neurodegeneration
KW - tryptophan
UR - http://www.scopus.com/inward/record.url?scp=85073037404&partnerID=8YFLogxK
U2 - 10.3389/fnins.2019.01013
DO - 10.3389/fnins.2019.01013
M3 - Review article
VL - 13
SP - 1
EP - 11
JO - Frontiers in Neuroscience
T2 - Frontiers in Neuroscience
JF - Frontiers in Neuroscience
SN - 1662-4548
M1 - 1013
ER -