The gut microbiome: a key player in the complexity of amyotrophic lateral sclerosis (ALS)

Background Much progress has been made in mapping genetic abnormalities linked to amyotrophic lateral sclerosis (ALS), but the majority of cases still present with no known underlying cause. Furthermore, even in families with a shared genetic abnormality there is significant phenotypic variability,...

Full description

Saved in:
Bibliographic Details
Published in:BMC medicine Vol. 19; no. 1; pp. 13 - 14
Main Authors: Boddy, Sarah L., Giovannelli, Ilaria, Sassani, Matilde, Cooper-Knock, Johnathan, Snyder, Michael P., Segal, Eran, Elinav, Eran, Barker, Lynne A., Shaw, Pamela J., McDermott, Christopher J.
Format: Journal Article
Language:English
Published: London BioMed Central 20.01.2021
BioMed Central Ltd
Springer Nature B.V
BMC
Subjects:
ISSN:1741-7015, 1741-7015
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Abstract Background Much progress has been made in mapping genetic abnormalities linked to amyotrophic lateral sclerosis (ALS), but the majority of cases still present with no known underlying cause. Furthermore, even in families with a shared genetic abnormality there is significant phenotypic variability, suggesting that non-genetic elements may modify pathogenesis. Identification of such disease-modifiers is important as they might represent new therapeutic targets. A growing body of research has begun to shed light on the role played by the gut microbiome in health and disease with a number of studies linking abnormalities to ALS. Main body The microbiome refers to the genes belonging to the myriad different microorganisms that live within and upon us, collectively known as the microbiota. Most of these microbes are found in the intestines, where they play important roles in digestion and the generation of key metabolites including neurotransmitters. The gut microbiota is an important aspect of the environment in which our bodies operate and inter-individual differences may be key to explaining the different disease outcomes seen in ALS. Work has begun to investigate animal models of the disease, and the gut microbiomes of people living with ALS, revealing changes in the microbial communities of these groups. The current body of knowledge will be summarised in this review. Advances in microbiome sequencing methods will be highlighted, as their improved resolution now enables researchers to further explore differences at a functional level. Proposed mechanisms connecting the gut microbiome to neurodegeneration will also be considered, including direct effects via metabolites released into the host circulation and indirect effects on bioavailability of nutrients and even medications. Conclusion Profiling of the gut microbiome has the potential to add an environmental component to rapidly advancing studies of ALS genetics and move research a step further towards personalised medicine for this disease. Moreover, should compelling evidence of upstream neurotoxicity or neuroprotection initiated by gut microbiota emerge, modification of the microbiome will represent a potential new avenue for disease modifying therapies. For an intractable condition with few current therapeutic options, further research into the ALS microbiome is of crucial importance.
AbstractList Much progress has been made in mapping genetic abnormalities linked to amyotrophic lateral sclerosis (ALS), but the majority of cases still present with no known underlying cause. Furthermore, even in families with a shared genetic abnormality there is significant phenotypic variability, suggesting that non-genetic elements may modify pathogenesis. Identification of such disease-modifiers is important as they might represent new therapeutic targets. A growing body of research has begun to shed light on the role played by the gut microbiome in health and disease with a number of studies linking abnormalities to ALS. Profiling of the gut microbiome has the potential to add an environmental component to rapidly advancing studies of ALS genetics and move research a step further towards personalised medicine for this disease. Moreover, should compelling evidence of upstream neurotoxicity or neuroprotection initiated by gut microbiota emerge, modification of the microbiome will represent a potential new avenue for disease modifying therapies. For an intractable condition with few current therapeutic options, further research into the ALS microbiome is of crucial importance.
Background Much progress has been made in mapping genetic abnormalities linked to amyotrophic lateral sclerosis (ALS), but the majority of cases still present with no known underlying cause. Furthermore, even in families with a shared genetic abnormality there is significant phenotypic variability, suggesting that non-genetic elements may modify pathogenesis. Identification of such disease-modifiers is important as they might represent new therapeutic targets. A growing body of research has begun to shed light on the role played by the gut microbiome in health and disease with a number of studies linking abnormalities to ALS. Main body The microbiome refers to the genes belonging to the myriad different microorganisms that live within and upon us, collectively known as the microbiota. Most of these microbes are found in the intestines, where they play important roles in digestion and the generation of key metabolites including neurotransmitters. The gut microbiota is an important aspect of the environment in which our bodies operate and inter-individual differences may be key to explaining the different disease outcomes seen in ALS. Work has begun to investigate animal models of the disease, and the gut microbiomes of people living with ALS, revealing changes in the microbial communities of these groups. The current body of knowledge will be summarised in this review. Advances in microbiome sequencing methods will be highlighted, as their improved resolution now enables researchers to further explore differences at a functional level. Proposed mechanisms connecting the gut microbiome to neurodegeneration will also be considered, including direct effects via metabolites released into the host circulation and indirect effects on bioavailability of nutrients and even medications. Conclusion Profiling of the gut microbiome has the potential to add an environmental component to rapidly advancing studies of ALS genetics and move research a step further towards personalised medicine for this disease. Moreover, should compelling evidence of upstream neurotoxicity or neuroprotection initiated by gut microbiota emerge, modification of the microbiome will represent a potential new avenue for disease modifying therapies. For an intractable condition with few current therapeutic options, further research into the ALS microbiome is of crucial importance.
Background Much progress has been made in mapping genetic abnormalities linked to amyotrophic lateral sclerosis (ALS), but the majority of cases still present with no known underlying cause. Furthermore, even in families with a shared genetic abnormality there is significant phenotypic variability, suggesting that non-genetic elements may modify pathogenesis. Identification of such disease-modifiers is important as they might represent new therapeutic targets. A growing body of research has begun to shed light on the role played by the gut microbiome in health and disease with a number of studies linking abnormalities to ALS. Main body The microbiome refers to the genes belonging to the myriad different microorganisms that live within and upon us, collectively known as the microbiota. Most of these microbes are found in the intestines, where they play important roles in digestion and the generation of key metabolites including neurotransmitters. The gut microbiota is an important aspect of the environment in which our bodies operate and inter-individual differences may be key to explaining the different disease outcomes seen in ALS. Work has begun to investigate animal models of the disease, and the gut microbiomes of people living with ALS, revealing changes in the microbial communities of these groups. The current body of knowledge will be summarised in this review. Advances in microbiome sequencing methods will be highlighted, as their improved resolution now enables researchers to further explore differences at a functional level. Proposed mechanisms connecting the gut microbiome to neurodegeneration will also be considered, including direct effects via metabolites released into the host circulation and indirect effects on bioavailability of nutrients and even medications. Conclusion Profiling of the gut microbiome has the potential to add an environmental component to rapidly advancing studies of ALS genetics and move research a step further towards personalised medicine for this disease. Moreover, should compelling evidence of upstream neurotoxicity or neuroprotection initiated by gut microbiota emerge, modification of the microbiome will represent a potential new avenue for disease modifying therapies. For an intractable condition with few current therapeutic options, further research into the ALS microbiome is of crucial importance. Keywords: Amyotrophic lateral sclerosis, ALS, Microbiome, Disease modifiers, Microbial metabolites, Microbial
Background Much progress has been made in mapping genetic abnormalities linked to amyotrophic lateral sclerosis (ALS), but the majority of cases still present with no known underlying cause. Furthermore, even in families with a shared genetic abnormality there is significant phenotypic variability, suggesting that non-genetic elements may modify pathogenesis. Identification of such disease-modifiers is important as they might represent new therapeutic targets. A growing body of research has begun to shed light on the role played by the gut microbiome in health and disease with a number of studies linking abnormalities to ALS. Main body The microbiome refers to the genes belonging to the myriad different microorganisms that live within and upon us, collectively known as the microbiota. Most of these microbes are found in the intestines, where they play important roles in digestion and the generation of key metabolites including neurotransmitters. The gut microbiota is an important aspect of the environment in which our bodies operate and inter-individual differences may be key to explaining the different disease outcomes seen in ALS. Work has begun to investigate animal models of the disease, and the gut microbiomes of people living with ALS, revealing changes in the microbial communities of these groups. The current body of knowledge will be summarised in this review. Advances in microbiome sequencing methods will be highlighted, as their improved resolution now enables researchers to further explore differences at a functional level. Proposed mechanisms connecting the gut microbiome to neurodegeneration will also be considered, including direct effects via metabolites released into the host circulation and indirect effects on bioavailability of nutrients and even medications. Conclusion Profiling of the gut microbiome has the potential to add an environmental component to rapidly advancing studies of ALS genetics and move research a step further towards personalised medicine for this disease. Moreover, should compelling evidence of upstream neurotoxicity or neuroprotection initiated by gut microbiota emerge, modification of the microbiome will represent a potential new avenue for disease modifying therapies. For an intractable condition with few current therapeutic options, further research into the ALS microbiome is of crucial importance.
Much progress has been made in mapping genetic abnormalities linked to amyotrophic lateral sclerosis (ALS), but the majority of cases still present with no known underlying cause. Furthermore, even in families with a shared genetic abnormality there is significant phenotypic variability, suggesting that non-genetic elements may modify pathogenesis. Identification of such disease-modifiers is important as they might represent new therapeutic targets. A growing body of research has begun to shed light on the role played by the gut microbiome in health and disease with a number of studies linking abnormalities to ALS. The microbiome refers to the genes belonging to the myriad different microorganisms that live within and upon us, collectively known as the microbiota. Most of these microbes are found in the intestines, where they play important roles in digestion and the generation of key metabolites including neurotransmitters. The gut microbiota is an important aspect of the environment in which our bodies operate and inter-individual differences may be key to explaining the different disease outcomes seen in ALS. Work has begun to investigate animal models of the disease, and the gut microbiomes of people living with ALS, revealing changes in the microbial communities of these groups. The current body of knowledge will be summarised in this review. Advances in microbiome sequencing methods will be highlighted, as their improved resolution now enables researchers to further explore differences at a functional level. Proposed mechanisms connecting the gut microbiome to neurodegeneration will also be considered, including direct effects via metabolites released into the host circulation and indirect effects on bioavailability of nutrients and even medications. Profiling of the gut microbiome has the potential to add an environmental component to rapidly advancing studies of ALS genetics and move research a step further towards personalised medicine for this disease. Moreover, should compelling evidence of upstream neurotoxicity or neuroprotection initiated by gut microbiota emerge, modification of the microbiome will represent a potential new avenue for disease modifying therapies. For an intractable condition with few current therapeutic options, further research into the ALS microbiome is of crucial importance.
Much progress has been made in mapping genetic abnormalities linked to amyotrophic lateral sclerosis (ALS), but the majority of cases still present with no known underlying cause. Furthermore, even in families with a shared genetic abnormality there is significant phenotypic variability, suggesting that non-genetic elements may modify pathogenesis. Identification of such disease-modifiers is important as they might represent new therapeutic targets. A growing body of research has begun to shed light on the role played by the gut microbiome in health and disease with a number of studies linking abnormalities to ALS.BACKGROUNDMuch progress has been made in mapping genetic abnormalities linked to amyotrophic lateral sclerosis (ALS), but the majority of cases still present with no known underlying cause. Furthermore, even in families with a shared genetic abnormality there is significant phenotypic variability, suggesting that non-genetic elements may modify pathogenesis. Identification of such disease-modifiers is important as they might represent new therapeutic targets. A growing body of research has begun to shed light on the role played by the gut microbiome in health and disease with a number of studies linking abnormalities to ALS.The microbiome refers to the genes belonging to the myriad different microorganisms that live within and upon us, collectively known as the microbiota. Most of these microbes are found in the intestines, where they play important roles in digestion and the generation of key metabolites including neurotransmitters. The gut microbiota is an important aspect of the environment in which our bodies operate and inter-individual differences may be key to explaining the different disease outcomes seen in ALS. Work has begun to investigate animal models of the disease, and the gut microbiomes of people living with ALS, revealing changes in the microbial communities of these groups. The current body of knowledge will be summarised in this review. Advances in microbiome sequencing methods will be highlighted, as their improved resolution now enables researchers to further explore differences at a functional level. Proposed mechanisms connecting the gut microbiome to neurodegeneration will also be considered, including direct effects via metabolites released into the host circulation and indirect effects on bioavailability of nutrients and even medications.MAIN BODYThe microbiome refers to the genes belonging to the myriad different microorganisms that live within and upon us, collectively known as the microbiota. Most of these microbes are found in the intestines, where they play important roles in digestion and the generation of key metabolites including neurotransmitters. The gut microbiota is an important aspect of the environment in which our bodies operate and inter-individual differences may be key to explaining the different disease outcomes seen in ALS. Work has begun to investigate animal models of the disease, and the gut microbiomes of people living with ALS, revealing changes in the microbial communities of these groups. The current body of knowledge will be summarised in this review. Advances in microbiome sequencing methods will be highlighted, as their improved resolution now enables researchers to further explore differences at a functional level. Proposed mechanisms connecting the gut microbiome to neurodegeneration will also be considered, including direct effects via metabolites released into the host circulation and indirect effects on bioavailability of nutrients and even medications.Profiling of the gut microbiome has the potential to add an environmental component to rapidly advancing studies of ALS genetics and move research a step further towards personalised medicine for this disease. Moreover, should compelling evidence of upstream neurotoxicity or neuroprotection initiated by gut microbiota emerge, modification of the microbiome will represent a potential new avenue for disease modifying therapies. For an intractable condition with few current therapeutic options, further research into the ALS microbiome is of crucial importance.CONCLUSIONProfiling of the gut microbiome has the potential to add an environmental component to rapidly advancing studies of ALS genetics and move research a step further towards personalised medicine for this disease. Moreover, should compelling evidence of upstream neurotoxicity or neuroprotection initiated by gut microbiota emerge, modification of the microbiome will represent a potential new avenue for disease modifying therapies. For an intractable condition with few current therapeutic options, further research into the ALS microbiome is of crucial importance.
Abstract Background Much progress has been made in mapping genetic abnormalities linked to amyotrophic lateral sclerosis (ALS), but the majority of cases still present with no known underlying cause. Furthermore, even in families with a shared genetic abnormality there is significant phenotypic variability, suggesting that non-genetic elements may modify pathogenesis. Identification of such disease-modifiers is important as they might represent new therapeutic targets. A growing body of research has begun to shed light on the role played by the gut microbiome in health and disease with a number of studies linking abnormalities to ALS. Main body The microbiome refers to the genes belonging to the myriad different microorganisms that live within and upon us, collectively known as the microbiota. Most of these microbes are found in the intestines, where they play important roles in digestion and the generation of key metabolites including neurotransmitters. The gut microbiota is an important aspect of the environment in which our bodies operate and inter-individual differences may be key to explaining the different disease outcomes seen in ALS. Work has begun to investigate animal models of the disease, and the gut microbiomes of people living with ALS, revealing changes in the microbial communities of these groups. The current body of knowledge will be summarised in this review. Advances in microbiome sequencing methods will be highlighted, as their improved resolution now enables researchers to further explore differences at a functional level. Proposed mechanisms connecting the gut microbiome to neurodegeneration will also be considered, including direct effects via metabolites released into the host circulation and indirect effects on bioavailability of nutrients and even medications. Conclusion Profiling of the gut microbiome has the potential to add an environmental component to rapidly advancing studies of ALS genetics and move research a step further towards personalised medicine for this disease. Moreover, should compelling evidence of upstream neurotoxicity or neuroprotection initiated by gut microbiota emerge, modification of the microbiome will represent a potential new avenue for disease modifying therapies. For an intractable condition with few current therapeutic options, further research into the ALS microbiome is of crucial importance.
ArticleNumber 13
Audience Academic
Author Sassani, Matilde
Barker, Lynne A.
Shaw, Pamela J.
Elinav, Eran
Boddy, Sarah L.
Segal, Eran
Snyder, Michael P.
Cooper-Knock, Johnathan
Giovannelli, Ilaria
McDermott, Christopher J.
Author_xml – sequence: 1
  givenname: Sarah L.
  surname: Boddy
  fullname: Boddy, Sarah L.
  organization: Sheffield Institute for Translational Neuroscience, University of Sheffield
– sequence: 2
  givenname: Ilaria
  surname: Giovannelli
  fullname: Giovannelli, Ilaria
  organization: Sheffield Institute for Translational Neuroscience, University of Sheffield
– sequence: 3
  givenname: Matilde
  surname: Sassani
  fullname: Sassani, Matilde
  organization: Sheffield Institute for Translational Neuroscience, University of Sheffield
– sequence: 4
  givenname: Johnathan
  surname: Cooper-Knock
  fullname: Cooper-Knock, Johnathan
  organization: Sheffield Institute for Translational Neuroscience, University of Sheffield
– sequence: 5
  givenname: Michael P.
  surname: Snyder
  fullname: Snyder, Michael P.
  organization: Stanford Center for Genomics and Personalized Medicine, Stanford University School of Medicine
– sequence: 6
  givenname: Eran
  surname: Segal
  fullname: Segal, Eran
  organization: Department of Computer Science and Applied Mathematics, Weizmann Institute of Science
– sequence: 7
  givenname: Eran
  surname: Elinav
  fullname: Elinav, Eran
  organization: Department of Immunology, Weizmann Institute of Science, Division of Cancer-Microbiome Research, DKFZ
– sequence: 8
  givenname: Lynne A.
  surname: Barker
  fullname: Barker, Lynne A.
  organization: Centre for Behavioural Science and Applied Psychology, Sheffield Hallam University
– sequence: 9
  givenname: Pamela J.
  surname: Shaw
  fullname: Shaw, Pamela J.
  organization: Sheffield Institute for Translational Neuroscience, University of Sheffield
– sequence: 10
  givenname: Christopher J.
  surname: McDermott
  fullname: McDermott, Christopher J.
  email: c.j.mcdermott@sheffield.ac.uk
  organization: Sheffield Institute for Translational Neuroscience, University of Sheffield
BackLink https://www.ncbi.nlm.nih.gov/pubmed/33468103$$D View this record in MEDLINE/PubMed
BookMark eNp9kstu1DAYhSNURC_wAiyQJSRUFim-xg4LpFHFpdJILCgLVpbt_JnxkMSDnSDm7fF0SjtToSoLR_Z3ju3jc1ocDWGAonhJ8AUhqnqXCK1JVWKKS0yUEiV7UpwQyUkpMRFHe__HxWlKK4ypkJI_K44Z45UimJ0UP66XgBbTiHrvYrA-9PAeGfQTNmjdmQ1E5Ac0ZsaFft3BHz9uUGiR6TdhjGG99A51ZoRoOpRcBzEkn9D5bP7t7fPiaWu6BC9ux7Pi-6eP15dfyvnXz1eXs3npKqbGUhgwrSUNkU5QB84JZYEzzqkQ1graCEVt41oKilhLRAstaSXnTGU9ocDOiqudbxPMSq-j703c6GC8vpkIcaFNHH0-nFY1VYwzKW1DeUMaixvMacWwpc6SmmavDzuv9WR7aBwMY77ZgenhyuCXehF-a6lIxaTIBue3BjH8miCNuvfJQdeZAcKUNOWy5pQqJTP6-gG6ClMcclSZqnHN6kqye2ph8gX80ObYjdua6lklMOeYUZKpi_9Q-Wsgv2tuTevz_IHgzZ5gCaYblyl00-jDkA7BV_uJ3EXxr0EZoDsg1yelCO0dQrDe1lTvaqpzTfVNTfVWpB6InB_NdvN8bt89LmU7acr7DAuI97E9ovoLmVn4xA
CitedBy_id crossref_primary_10_3390_ijms26178419
crossref_primary_10_3390_biom11101441
crossref_primary_10_3390_molecules29246026
crossref_primary_10_5937_arhfarm74_46612
crossref_primary_10_1038_s41598_024_75083_z
crossref_primary_10_1186_s12916_024_03781_6
crossref_primary_10_3390_ijms232213665
crossref_primary_10_1039_D5NP00021A
crossref_primary_10_3390_nu16050590
crossref_primary_10_1007_s12035_025_04747_2
crossref_primary_10_1186_s13099_025_00696_2
crossref_primary_10_1002_cph4_70009
crossref_primary_10_3390_ijms25031871
crossref_primary_10_1021_acschemneuro_5c00254
crossref_primary_10_3389_fonc_2022_926920
crossref_primary_10_3390_cimb46050271
crossref_primary_10_1097_WCO_0000000000000983
crossref_primary_10_1097_WCO_0000000000000986
crossref_primary_10_1038_s41598_022_25033_4
crossref_primary_10_1186_s13024_022_00525_z
crossref_primary_10_3390_brainsci12111579
crossref_primary_10_1002_ana_27208
crossref_primary_10_3390_biomedicines11030827
crossref_primary_10_1007_s11010_023_04853_6
crossref_primary_10_3390_biomedicines11030748
crossref_primary_10_1016_j_lfs_2021_120156
crossref_primary_10_1038_s41582_024_00991_7
crossref_primary_10_1007_s12035_024_04228_y
crossref_primary_10_3390_diagnostics12071742
crossref_primary_10_1016_j_biopha_2024_117588
crossref_primary_10_1016_j_jclinane_2025_111801
crossref_primary_10_1038_s41582_023_00867_2
crossref_primary_10_1155_2022_3300903
crossref_primary_10_3390_ijms23063253
crossref_primary_10_1007_s12017_025_08870_0
crossref_primary_10_3390_ijms24119577
crossref_primary_10_3389_fneur_2023_1133546
crossref_primary_10_3390_biom14091138
crossref_primary_10_1038_s41598_024_68645_8
crossref_primary_10_1177_19714009251345102
crossref_primary_10_1016_j_lfs_2023_122022
crossref_primary_10_3390_biomedicines9070753
crossref_primary_10_1007_s12035_023_03568_5
crossref_primary_10_3390_medicina61091694
crossref_primary_10_1186_s12974_023_03007_1
crossref_primary_10_1080_21678421_2024_2433578
crossref_primary_10_1007_s12035_024_04269_3
crossref_primary_10_3390_ijms26083658
crossref_primary_10_3390_brainsci14050471
crossref_primary_10_3390_jcm12041650
crossref_primary_10_1093_brain_awad306
crossref_primary_10_3389_fneur_2021_788462
crossref_primary_10_3390_life13102023
crossref_primary_10_4103_1673_5374_382223
crossref_primary_10_3390_microbiolres15020033
crossref_primary_10_1016_j_phrs_2022_106377
crossref_primary_10_1212_WNL_0000000000207367
crossref_primary_10_1002_ana_27126
crossref_primary_10_1007_s12035_025_04830_8
crossref_primary_10_1016_j_neurot_2024_e00469
crossref_primary_10_1016_j_neurot_2024_e00441
crossref_primary_10_1111_joim_13336
crossref_primary_10_1186_s40035_021_00272_z
crossref_primary_10_3389_fnins_2022_1002266
crossref_primary_10_1186_s12974_022_02421_1
crossref_primary_10_3389_fneur_2023_1289467
crossref_primary_10_1007_s12640_023_00681_0
crossref_primary_10_1016_j_arr_2024_102504
crossref_primary_10_3390_ijms23094504
crossref_primary_10_3390_ijms26157211
crossref_primary_10_1016_j_neurot_2024_e00478
crossref_primary_10_3390_ijms23031184
crossref_primary_10_1186_s40659_024_00505_1
crossref_primary_10_1016_j_jnutbio_2024_109622
crossref_primary_10_1038_s41582_023_00845_8
crossref_primary_10_4103_1673_5374_335151
crossref_primary_10_1111_jgh_16650
Cites_doi 10.1038/nm.4106
10.1038/nature25973
10.1016/j.nbd.2006.12.015
10.1097/00003246-200004001-00007
10.1186/s40478-019-0797-0
10.1517/17425255.4.9.1223
10.1126/science.1166066
10.1016/j.clinthera.2016.12.014
10.1038/s41575-018-0061-2
10.3389/fphar.2018.01354
10.1016/j.nbd.2017.12.006
10.1038/nature12726
10.1186/s40168-018-0551-z
10.3389/fmicb.2018.02013
10.1016/s0022-510x(01)00613-x
10.1038/s41598-020-69845-8
10.1002/mnfr.201801187
10.1113/jphysiol.1985.sp015882
10.1080/21678421.2020.1772825
10.4199/C00093ED1V01Y201309GMM004
10.1038/s41586-019-1443-5
10.1002/jcp.25518
10.1007/s11481-012-9426-4
10.1038/nature08821
10.1038/s41597-020-0427-5
10.14814/phy2.13443
10.1186/s12974-019-1434-3
10.1073/pnas.1314085111
10.1212/wnl.0000000000005996
10.1016/j.jnutbio.2010.07.009
10.1016/j.nutres.2008.02.012
10.1016/j.cell.2014.06.034
10.3390/ijms20040974
10.1093/epirev/mxu001
10.1016/j.neulet.2017.06.052
10.14814/phy2.12356
10.1212/WNL.50.1.66
10.3389/fmicb.2016.01479
10.1002/ncp.10489
10.1038/s41467-019-08294-y
10.1038/nri.2016.42
10.1007/s13311-017-0585-0
10.3389/fpsyt.2019.00034
10.1016/j.neurobiolaging.2017.09.023
10.1007/s00401-014-1251-9
10.1016/j.cell.2014.03.011
10.1007/s00394-017-1445-8
10.1038/nature05414
10.1111/nan.12520
10.3389/fnins.2019.00171
10.1289/ehp.0900580
10.1001/jamaneurol.2016.0594
10.1080/00365520802321212
10.3389/fneur.2019.01021
10.1016/j.cell.2013.12.016
10.1111/ene.13986
10.1126/science.1154584
10.1038/nature12721
10.1016/j.chom.2015.04.011
10.1016/j.neuron.2011.09.010
10.1038/362059a0
10.1038/nbt.2676
10.1212/01.wnl.0000078320.18564.9f
10.1038/nn.4476
10.3390/ijms21114045
10.1152/ajpgi.00574.2004
10.1182/blood-2018-11-844555
10.1159/000453359
10.1177/0884533611436116
10.1186/s12916-020-01607-9
10.1038/nrneurol.2016.111
10.1016/j.jaci.2020.04.037
10.3389/fimmu.2017.01630
10.3390/nu11040923
10.1038/s41586-019-1291-3
10.1016/j.ncl.2015.07.010
10.7150/ijbs.11084
10.1016/j.neuron.2011.09.011
10.3389/fmicb.2016.00459
10.1053/j.gastro.2015.10.005
10.1111/j.1471-4159.2012.07955.x
10.1016/j.jep.2005.12.032
10.1038/s41598-019-42227-5
10.1242/dmm.041947
10.30802/AALAS-CM-18-000039
10.1038/s41586-020-2288-7
10.1016/j.ygeno.2012.07.012
10.1056/NEJM199403033300901
10.1038/nn.4030
10.3109/17482960802566824
10.1126/science.aad9378
10.1126/science.1241214
10.1097/cm9.0000000000000351
10.1038/nrmicro2536
10.1186/s40478-017-0424-x
10.1038/nrd4609
10.1111/imm.13158
ContentType Journal Article
Copyright The Author(s) 2021
COPYRIGHT 2021 BioMed Central Ltd.
2021. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
Copyright_xml – notice: The Author(s) 2021
– notice: COPYRIGHT 2021 BioMed Central Ltd.
– notice: 2021. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
DBID C6C
AAYXX
CITATION
NPM
3V.
7QL
7U9
7X7
7XB
88E
8FI
8FJ
8FK
ABUWG
AFKRA
AZQEC
BENPR
C1K
CCPQU
DWQXO
FYUFA
GHDGH
H94
K9.
M0S
M1P
M7N
PHGZM
PHGZT
PIMPY
PJZUB
PKEHL
PPXIY
PQEST
PQQKQ
PQUKI
PRINS
7X8
5PM
DOA
DOI 10.1186/s12916-020-01885-3
DatabaseName Springer Nature Link
CrossRef
PubMed
ProQuest Central (Corporate)
Bacteriology Abstracts (Microbiology B)
Virology and AIDS Abstracts
Health & Medical Collection
ProQuest Central (purchase pre-March 2016)
Medical Database (Alumni Edition)
Hospital Premium Collection
Hospital Premium Collection (Alumni Edition)
ProQuest Central (Alumni) (purchase pre-March 2016)
ProQuest Central
ProQuest Central UK/Ireland
ProQuest Central Essentials
ProQuest Central
Environmental Sciences and Pollution Management
ProQuest One Community College
ProQuest Central Korea
Health Research Premium Collection
Health Research Premium Collection (Alumni)
AIDS and Cancer Research Abstracts
ProQuest Health & Medical Complete (Alumni)
Health & Medical Collection (Alumni Edition)
Medical Database
Algology Mycology and Protozoology Abstracts (Microbiology C)
ProQuest Central Premium
ProQuest One Academic (New)
ProQuest Publicly Available Content Database
ProQuest Health & Medical Research Collection
ProQuest One Academic Middle East (New)
ProQuest One Health & Nursing
ProQuest One Academic Eastern Edition (DO NOT USE)
ProQuest One Academic (retired)
ProQuest One Academic UKI Edition
ProQuest Central China
MEDLINE - Academic
PubMed Central (Full Participant titles)
DOAJ Directory of Open Access Journals
DatabaseTitle CrossRef
PubMed
Publicly Available Content Database
ProQuest One Academic Middle East (New)
ProQuest Central Essentials
ProQuest Health & Medical Complete (Alumni)
ProQuest Central (Alumni Edition)
ProQuest One Community College
ProQuest One Health & Nursing
ProQuest Central China
Environmental Sciences and Pollution Management
ProQuest Central
ProQuest Health & Medical Research Collection
Health Research Premium Collection
Health and Medicine Complete (Alumni Edition)
ProQuest Central Korea
Bacteriology Abstracts (Microbiology B)
Algology Mycology and Protozoology Abstracts (Microbiology C)
Health & Medical Research Collection
AIDS and Cancer Research Abstracts
ProQuest Central (New)
ProQuest Medical Library (Alumni)
Virology and AIDS Abstracts
ProQuest One Academic Eastern Edition
ProQuest Hospital Collection
Health Research Premium Collection (Alumni)
ProQuest Hospital Collection (Alumni)
ProQuest Health & Medical Complete
ProQuest Medical Library
ProQuest One Academic UKI Edition
ProQuest One Academic
ProQuest One Academic (New)
ProQuest Central (Alumni)
MEDLINE - Academic
DatabaseTitleList


Publicly Available Content Database

PubMed
MEDLINE - Academic

Database_xml – sequence: 1
  dbid: DOA
  name: DOAJ Open Access Journals
  url: https://www.doaj.org/
  sourceTypes: Open Website
– sequence: 2
  dbid: NPM
  name: PubMed
  url: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed
  sourceTypes: Index Database
– sequence: 3
  dbid: PIMPY
  name: Publicly Available Content Database
  url: http://search.proquest.com/publiccontent
  sourceTypes: Aggregation Database
DeliveryMethod fulltext_linktorsrc
Discipline Medicine
EISSN 1741-7015
EndPage 14
ExternalDocumentID oai_doaj_org_article_892834377bd24d1db0d042630b2cb192
PMC7816375
A650440321
33468103
10_1186_s12916_020_01885_3
Genre Journal Article
Review
GeographicLocations United States
GeographicLocations_xml – name: United States
GrantInformation_xml – fundername: European Research Council
– fundername: UK Research and Innovation (GB)
– fundername: NIHR Sheffield Biomedical Research Centre (GB)
– fundername: University of Sheffield (GB)
– fundername: NIHR Oxford Biomedical Research Centre (GB)
– fundername: Howard Hughes Medical Institute
  funderid: http://dx.doi.org/10.13039/100000011
– fundername: Medical Research Council (GB)
– fundername: NIH Human Microbiome Project
  grantid: 1U54DE02378901
– fundername: Bill & Melinda Gates Foundation
– fundername: Wellcome Trust
  funderid: http://dx.doi.org/10.13039/100010269
– fundername: ;
– fundername: ;
  grantid: 1U54DE02378901
GroupedDBID ---
0R~
23N
2WC
4.4
53G
5GY
5VS
6J9
6PF
7X7
88E
8FI
8FJ
AAFWJ
AAJSJ
AASML
AAWTL
ABDBF
ABUWG
ACGFO
ACGFS
ACIHN
ACPRK
ACUHS
ADBBV
ADRAZ
ADUKV
AEAQA
AENEX
AFKRA
AFPKN
AFRAH
AHBYD
AHMBA
AHYZX
ALMA_UNASSIGNED_HOLDINGS
AMKLP
AMTXH
AOIJS
BAPOH
BAWUL
BCNDV
BENPR
BFQNJ
BMC
BPHCQ
BVXVI
C6C
CCPQU
CS3
DIK
DU5
E3Z
EAD
EAP
EAS
EBD
EBLON
EBS
EMB
EMK
EMOBN
ESX
F5P
FYUFA
GROUPED_DOAJ
GX1
HMCUK
HYE
IAO
IHR
IHW
INH
INR
ITC
KQ8
M1P
M48
MK0
M~E
O5R
O5S
OK1
OVT
P2P
PGMZT
PHGZM
PHGZT
PIMPY
PJZUB
PPXIY
PQQKQ
PROAC
PSQYO
PUEGO
RBZ
RNS
ROL
RPM
RSV
SMD
SOJ
SV3
TR2
TUS
UKHRP
WOQ
WOW
XSB
AAYXX
AFFHD
CITATION
-5E
-5G
-A0
-BR
3V.
ACRMQ
ADINQ
ALIPV
C24
NPM
7QL
7U9
7XB
8FK
AZQEC
C1K
DWQXO
H94
K9.
M7N
PKEHL
PQEST
PQUKI
PRINS
7X8
5PM
ID FETCH-LOGICAL-c638t-5aeafb1d17c52cecc58be4344255bb52d582bdcf2e81bb15fef1f74438c6312e3
IEDL.DBID BENPR
ISICitedReferencesCount 91
ISICitedReferencesURI http://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=Summon&SrcAuth=ProQuest&DestLinkType=CitingArticles&DestApp=WOS_CPL&KeyUT=000609364600001&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D
ISSN 1741-7015
IngestDate Fri Oct 03 12:50:44 EDT 2025
Tue Nov 04 01:56:21 EST 2025
Thu Oct 02 09:15:05 EDT 2025
Wed Oct 08 14:21:21 EDT 2025
Tue Nov 11 10:37:04 EST 2025
Tue Nov 04 17:19:29 EST 2025
Thu May 22 21:21:14 EDT 2025
Thu Jan 02 22:57:49 EST 2025
Sat Nov 29 04:08:22 EST 2025
Tue Nov 18 21:01:46 EST 2025
Sat Sep 06 07:29:20 EDT 2025
IsDoiOpenAccess true
IsOpenAccess true
IsPeerReviewed true
IsScholarly true
Issue 1
Keywords ALS
Disease modifiers
Amyotrophic lateral sclerosis
Microbial
Microbial metabolites
Microbiome
Language English
License Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
LinkModel DirectLink
MergedId FETCHMERGED-LOGICAL-c638t-5aeafb1d17c52cecc58be4344255bb52d582bdcf2e81bb15fef1f74438c6312e3
Notes ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 14
ObjectType-Review-3
content type line 23
OpenAccessLink https://www.proquest.com/docview/2490939673?pq-origsite=%requestingapplication%
PMID 33468103
PQID 2490939673
PQPubID 42775
PageCount 14
ParticipantIDs doaj_primary_oai_doaj_org_article_892834377bd24d1db0d042630b2cb192
pubmedcentral_primary_oai_pubmedcentral_nih_gov_7816375
proquest_miscellaneous_2479422887
proquest_journals_2490939673
gale_infotracmisc_A650440321
gale_infotracacademiconefile_A650440321
gale_healthsolutions_A650440321
pubmed_primary_33468103
crossref_primary_10_1186_s12916_020_01885_3
crossref_citationtrail_10_1186_s12916_020_01885_3
springer_journals_10_1186_s12916_020_01885_3
PublicationCentury 2000
PublicationDate 2021-01-20
PublicationDateYYYYMMDD 2021-01-20
PublicationDate_xml – month: 01
  year: 2021
  text: 2021-01-20
  day: 20
PublicationDecade 2020
PublicationPlace London
PublicationPlace_xml – name: London
– name: England
PublicationTitle BMC medicine
PublicationTitleAbbrev BMC Med
PublicationTitleAlternate BMC Med
PublicationYear 2021
Publisher BioMed Central
BioMed Central Ltd
Springer Nature B.V
BMC
Publisher_xml – name: BioMed Central
– name: BioMed Central Ltd
– name: Springer Nature B.V
– name: BMC
References M Usami (1885_CR62) 2008; 28
1885_CR73
R Alonso (1885_CR38) 2015; 11
R Vangoitsenhoven (1885_CR71) 2020; 35
K Meyer (1885_CR78) 2014; 111
TJ Kwiatkowski Jr (1885_CR3) 2009; 323
J Cooper-Knock (1885_CR8) 2014; 127
MGI Langille (1885_CR45) 2013; 31
D Erny (1885_CR76) 2015; 18
VK Ridaura (1885_CR83) 2013; 341
R Mittal (1885_CR49) 2017; 232
1885_CR80
G Bensimon (1885_CR86) 1994; 330
1885_CR85
M Zhang (1885_CR66) 2000; 28
J Sun (1885_CR37) 2019; 26
M Zhuang (1885_CR96) 2019; 63
C-D Zhai (1885_CR31) 2019; 132
MG Rooks (1885_CR72) 2016; 16
A Chiò (1885_CR9) 2018; 91
J Cooper-Knock (1885_CR77) 2017; 5
Q Ma (1885_CR52) 2019; 16
B Tilocca (1885_CR47) 2020; 21
DR Rosen (1885_CR2) 1993; 362
BP Willing (1885_CR36) 2011; 9
J Sreedharan (1885_CR4) 2008; 319
ML Soliman (1885_CR60) 2013; 8
J Qin (1885_CR19) 2010; 464
PJ Turnbaugh (1885_CR84) 2006; 444
Y Belkaid (1885_CR70) 2014; 157
D Zhang (1885_CR61) 2019; 133
DW Dickson (1885_CR25) 2019; 7
S Wu (1885_CR21) 2015; 3
SG Cheung (1885_CR92) 2019; 10
1885_CR15
M DeJesus-Hernandez (1885_CR5) 2011; 72
1885_CR7
MM Haney (1885_CR24) 2018; 68
SA Banack (1885_CR11) 2003; 61
J Mandrioli (1885_CR79) 2019; 10
V Rothhammer (1885_CR64) 2016; 22
H Jeong (1885_CR43) 2019; 9
F Fang (1885_CR14) 2009; 117
I Rowland (1885_CR53) 2018; 57
M Mills (1885_CR82) 2019; 11
1885_CR29
A Lerner (1885_CR40) 2017; 8
E Blacher (1885_CR17) 2019; 572
J Mas-Lloret (1885_CR46) 2020; 7
M Benatar (1885_CR26) 2007; 26
SA Banack (1885_CR12) 2006; 106
1885_CR30
EF Smith (1885_CR68) 2019; 710
1885_CR34
1885_CR33
G Lach (1885_CR90) 2018; 15
D Rothschild (1885_CR100) 2018; 555
MJ Waring (1885_CR27) 2015; 14
T Gensollen (1885_CR69) 2016; 352
TR Sampson (1885_CR75) 2015; 17
1885_CR39
IW Mak (1885_CR28) 2014; 6
JD Beard (1885_CR13) 2015; 37
D Brenner (1885_CR32) 2018; 61
P Cimermancic (1885_CR48) 2014; 158
C Figueroa-Romero (1885_CR23) 2020; 13
N Zmora (1885_CR81) 2019; 16
R Krajmalnik-Brown (1885_CR54) 2012; 27
CE Jackson (1885_CR93) 2015; 33
H Abrahamsson (1885_CR94) 2008; 43
EV Hobson (1885_CR99) 2016; 12
T Yajima (1885_CR95) 1985; 368
AE Renton (1885_CR6) 2011; 72
AS Andrew (1885_CR10) 2017; 17
N Arpaia (1885_CR59) 2013; 504
M Pimentel (1885_CR97) 2006; 290
R Sitaraman (1885_CR42) 2018; 6
F De Vadder (1885_CR50) 2014; 156
GJ Groeneveld (1885_CR88) 2001; 191
1885_CR55
Y Furusawa (1885_CR58) 2013; 504
JP Karl (1885_CR91) 2018; 9
J Kehrmann (1885_CR74) 2020; 159
L Liu (1885_CR41) 2012; 100
TC Fung (1885_CR51) 2017; 20
Y-G Zhang (1885_CR22) 2017; 39
A Chio (1885_CR1) 2009; 10
JS Bell (1885_CR20) 2019; 45
ML Soliman (1885_CR57) 2012; 123
M Zimmermann (1885_CR87) 2019; 570
CA Zarate (1885_CR89) 2008; 4
1885_CR67
1885_CR65
G Parthasarathy (1885_CR98) 2016; 150
MAR Vinolo (1885_CR63) 2011; 22
Q Zeng (1885_CR35) 2020; 10
F-C Su (1885_CR16) 2016; 73
A Burberry (1885_CR18) 2020; 582
P Wang (1885_CR56) 2018; 111
J Jovel (1885_CR44) 2016; 7
References_xml – volume: 22
  start-page: 586
  year: 2016
  ident: 1885_CR64
  publication-title: Nat Med
  doi: 10.1038/nm.4106
– volume: 555
  start-page: 210
  year: 2018
  ident: 1885_CR100
  publication-title: Nature.
  doi: 10.1038/nature25973
– volume: 26
  start-page: 1
  year: 2007
  ident: 1885_CR26
  publication-title: Neurobiol Dis
  doi: 10.1016/j.nbd.2006.12.015
– volume: 28
  start-page: N60
  issue: 4 Suppl
  year: 2000
  ident: 1885_CR66
  publication-title: Crit Care Med
  doi: 10.1097/00003246-200004001-00007
– volume: 7
  start-page: 150
  year: 2019
  ident: 1885_CR25
  publication-title: Acta Neuropathol Commun
  doi: 10.1186/s40478-019-0797-0
– volume: 4
  start-page: 1223
  year: 2008
  ident: 1885_CR89
  publication-title: Expert Opin Drug Metab Toxicol
  doi: 10.1517/17425255.4.9.1223
– volume: 323
  start-page: 1205
  year: 2009
  ident: 1885_CR3
  publication-title: Science.
  doi: 10.1126/science.1166066
– volume: 39
  start-page: 322
  year: 2017
  ident: 1885_CR22
  publication-title: Clin Ther
  doi: 10.1016/j.clinthera.2016.12.014
– volume: 16
  start-page: 35
  year: 2019
  ident: 1885_CR81
  publication-title: Nat Rev Gastroenterol Hepatol
  doi: 10.1038/s41575-018-0061-2
– ident: 1885_CR73
  doi: 10.3389/fphar.2018.01354
– volume: 111
  start-page: 12
  year: 2018
  ident: 1885_CR56
  publication-title: Neurobiol Dis
  doi: 10.1016/j.nbd.2017.12.006
– volume: 504
  start-page: 451
  year: 2013
  ident: 1885_CR59
  publication-title: Nature
  doi: 10.1038/nature12726
– volume: 6
  start-page: 163
  year: 2018
  ident: 1885_CR42
  publication-title: Microbiome.
  doi: 10.1186/s40168-018-0551-z
– ident: 1885_CR80
– volume: 9
  start-page: 2013
  year: 2018
  ident: 1885_CR91
  publication-title: Front Microbiol
  doi: 10.3389/fmicb.2018.02013
– volume: 191
  start-page: 121
  year: 2001
  ident: 1885_CR88
  publication-title: J Neurol Sci
  doi: 10.1016/s0022-510x(01)00613-x
– volume: 10
  start-page: 12998
  year: 2020
  ident: 1885_CR35
  publication-title: Sci Rep
  doi: 10.1038/s41598-020-69845-8
– volume: 63
  start-page: 1801187
  year: 2019
  ident: 1885_CR96
  publication-title: Mol Nutr Food Res
  doi: 10.1002/mnfr.201801187
– volume: 368
  start-page: 667
  year: 1985
  ident: 1885_CR95
  publication-title: J Physiol
  doi: 10.1113/jphysiol.1985.sp015882
– ident: 1885_CR34
  doi: 10.1080/21678421.2020.1772825
– ident: 1885_CR15
  doi: 10.4199/C00093ED1V01Y201309GMM004
– volume: 572
  start-page: 474
  year: 2019
  ident: 1885_CR17
  publication-title: Nature.
  doi: 10.1038/s41586-019-1443-5
– volume: 232
  start-page: 2359
  year: 2017
  ident: 1885_CR49
  publication-title: J Cell Physiol
  doi: 10.1002/jcp.25518
– volume: 8
  start-page: 287
  year: 2013
  ident: 1885_CR60
  publication-title: J NeuroImmune Pharmacol
  doi: 10.1007/s11481-012-9426-4
– volume: 464
  start-page: 59
  year: 2010
  ident: 1885_CR19
  publication-title: Nature.
  doi: 10.1038/nature08821
– volume: 7
  start-page: 92
  year: 2020
  ident: 1885_CR46
  publication-title: Sci Data
  doi: 10.1038/s41597-020-0427-5
– ident: 1885_CR30
  doi: 10.14814/phy2.13443
– volume: 16
  start-page: 53
  year: 2019
  ident: 1885_CR52
  publication-title: J Neuroinflammation
  doi: 10.1186/s12974-019-1434-3
– volume: 111
  start-page: 829
  year: 2014
  ident: 1885_CR78
  publication-title: Proc Natl Acad Sci U S A
  doi: 10.1073/pnas.1314085111
– volume: 91
  start-page: e635
  year: 2018
  ident: 1885_CR9
  publication-title: Neurology.
  doi: 10.1212/wnl.0000000000005996
– volume: 22
  start-page: 849
  year: 2011
  ident: 1885_CR63
  publication-title: J Nutr Biochem
  doi: 10.1016/j.jnutbio.2010.07.009
– volume: 28
  start-page: 321
  year: 2008
  ident: 1885_CR62
  publication-title: Nutr Res
  doi: 10.1016/j.nutres.2008.02.012
– volume: 158
  start-page: 412
  year: 2014
  ident: 1885_CR48
  publication-title: Cell.
  doi: 10.1016/j.cell.2014.06.034
– ident: 1885_CR67
  doi: 10.3390/ijms20040974
– volume: 37
  start-page: 55
  year: 2015
  ident: 1885_CR13
  publication-title: Epidemiol Rev
  doi: 10.1093/epirev/mxu001
– volume: 710
  start-page: 132933
  year: 2019
  ident: 1885_CR68
  publication-title: Neurosci Lett
  doi: 10.1016/j.neulet.2017.06.052
– volume: 3
  start-page: e12356
  year: 2015
  ident: 1885_CR21
  publication-title: Physiol Rep
  doi: 10.14814/phy2.12356
– ident: 1885_CR85
  doi: 10.1212/WNL.50.1.66
– ident: 1885_CR7
– ident: 1885_CR29
  doi: 10.3389/fmicb.2016.01479
– volume: 35
  start-page: 406
  year: 2020
  ident: 1885_CR71
  publication-title: Nutr Clin Pract
  doi: 10.1002/ncp.10489
– ident: 1885_CR55
  doi: 10.1038/s41467-019-08294-y
– volume: 16
  start-page: 341
  year: 2016
  ident: 1885_CR72
  publication-title: Nat Rev Immunol
  doi: 10.1038/nri.2016.42
– volume: 15
  start-page: 36
  year: 2018
  ident: 1885_CR90
  publication-title: Neurotherapeutics.
  doi: 10.1007/s13311-017-0585-0
– volume: 10
  start-page: 34
  year: 2019
  ident: 1885_CR92
  publication-title: Front Psychiatry
  doi: 10.3389/fpsyt.2019.00034
– volume: 61
  start-page: 132
  year: 2018
  ident: 1885_CR32
  publication-title: Neurobiol Aging
  doi: 10.1016/j.neurobiolaging.2017.09.023
– volume: 127
  start-page: 333
  year: 2014
  ident: 1885_CR8
  publication-title: Acta Neuropathol
  doi: 10.1007/s00401-014-1251-9
– volume: 157
  start-page: 121
  year: 2014
  ident: 1885_CR70
  publication-title: Cell.
  doi: 10.1016/j.cell.2014.03.011
– volume: 57
  start-page: 1
  year: 2018
  ident: 1885_CR53
  publication-title: Eur J Nutr
  doi: 10.1007/s00394-017-1445-8
– volume: 444
  start-page: 1027
  year: 2006
  ident: 1885_CR84
  publication-title: Nature.
  doi: 10.1038/nature05414
– volume: 45
  start-page: 195
  year: 2019
  ident: 1885_CR20
  publication-title: Neuropathol Appl Neurobiol
  doi: 10.1111/nan.12520
– ident: 1885_CR39
  doi: 10.3389/fnins.2019.00171
– volume: 117
  start-page: 1387
  year: 2009
  ident: 1885_CR14
  publication-title: Environ Health Perspect
  doi: 10.1289/ehp.0900580
– volume: 73
  start-page: 803
  year: 2016
  ident: 1885_CR16
  publication-title: JAMA Neurol
  doi: 10.1001/jamaneurol.2016.0594
– volume: 43
  start-page: 1483
  year: 2008
  ident: 1885_CR94
  publication-title: Scand J Gastroenterol
  doi: 10.1080/00365520802321212
– volume: 10
  start-page: 1021
  year: 2019
  ident: 1885_CR79
  publication-title: Front Neurol
  doi: 10.3389/fneur.2019.01021
– volume: 156
  start-page: 84
  year: 2014
  ident: 1885_CR50
  publication-title: Cell.
  doi: 10.1016/j.cell.2013.12.016
– volume: 26
  start-page: 1355
  year: 2019
  ident: 1885_CR37
  publication-title: Eur J Neurol
  doi: 10.1111/ene.13986
– volume: 319
  start-page: 1668
  year: 2008
  ident: 1885_CR4
  publication-title: Science.
  doi: 10.1126/science.1154584
– volume: 504
  start-page: 446
  year: 2013
  ident: 1885_CR58
  publication-title: Nature.
  doi: 10.1038/nature12721
– volume: 17
  start-page: 565
  year: 2015
  ident: 1885_CR75
  publication-title: Cell Host Microbe
  doi: 10.1016/j.chom.2015.04.011
– volume: 72
  start-page: 257
  year: 2011
  ident: 1885_CR6
  publication-title: Neuron.
  doi: 10.1016/j.neuron.2011.09.010
– volume: 362
  start-page: 59
  year: 1993
  ident: 1885_CR2
  publication-title: Nature.
  doi: 10.1038/362059a0
– volume: 31
  start-page: 814
  year: 2013
  ident: 1885_CR45
  publication-title: Nat Biotechnol
  doi: 10.1038/nbt.2676
– volume: 61
  start-page: 387
  year: 2003
  ident: 1885_CR11
  publication-title: Neurology
  doi: 10.1212/01.wnl.0000078320.18564.9f
– volume: 20
  start-page: 145
  year: 2017
  ident: 1885_CR51
  publication-title: Nat Neurosci
  doi: 10.1038/nn.4476
– volume: 21
  start-page: 4045
  year: 2020
  ident: 1885_CR47
  publication-title: Int J Mol Sci
  doi: 10.3390/ijms21114045
– volume: 290
  start-page: G1089
  year: 2006
  ident: 1885_CR97
  publication-title: Am J Physiol Gastrointest Liver Physiol
  doi: 10.1152/ajpgi.00574.2004
– volume: 133
  start-page: 2168
  year: 2019
  ident: 1885_CR61
  publication-title: Blood.
  doi: 10.1182/blood-2018-11-844555
– volume: 17
  start-page: 110
  year: 2017
  ident: 1885_CR10
  publication-title: Neurodegener Dis
  doi: 10.1159/000453359
– volume: 27
  start-page: 201
  year: 2012
  ident: 1885_CR54
  publication-title: Nutr Clin Pract
  doi: 10.1177/0884533611436116
– ident: 1885_CR33
  doi: 10.1186/s12916-020-01607-9
– volume: 12
  start-page: 526
  year: 2016
  ident: 1885_CR99
  publication-title: Nat Rev Neurol
  doi: 10.1038/nrneurol.2016.111
– ident: 1885_CR65
  doi: 10.1016/j.jaci.2020.04.037
– volume: 8
  start-page: 1630
  year: 2017
  ident: 1885_CR40
  publication-title: Front Immunol
  doi: 10.3389/fimmu.2017.01630
– volume: 11
  start-page: 923
  year: 2019
  ident: 1885_CR82
  publication-title: Nutrients
  doi: 10.3390/nu11040923
– volume: 570
  start-page: 462
  year: 2019
  ident: 1885_CR87
  publication-title: Nature.
  doi: 10.1038/s41586-019-1291-3
– volume: 33
  start-page: 889
  year: 2015
  ident: 1885_CR93
  publication-title: Neurol Clin
  doi: 10.1016/j.ncl.2015.07.010
– volume: 11
  start-page: 546
  year: 2015
  ident: 1885_CR38
  publication-title: Int J Biol Sci
  doi: 10.7150/ijbs.11084
– volume: 72
  start-page: 245
  year: 2011
  ident: 1885_CR5
  publication-title: Neuron.
  doi: 10.1016/j.neuron.2011.09.011
– volume: 7
  start-page: 459
  year: 2016
  ident: 1885_CR44
  publication-title: Front Microbiol
  doi: 10.3389/fmicb.2016.00459
– volume: 150
  start-page: 367
  year: 2016
  ident: 1885_CR98
  publication-title: Gastroenterology
  doi: 10.1053/j.gastro.2015.10.005
– volume: 123
  start-page: 555
  year: 2012
  ident: 1885_CR57
  publication-title: J Neurochem
  doi: 10.1111/j.1471-4159.2012.07955.x
– volume: 106
  start-page: 97
  year: 2006
  ident: 1885_CR12
  publication-title: J Ethnopharmacol
  doi: 10.1016/j.jep.2005.12.032
– volume: 9
  start-page: 5953
  year: 2019
  ident: 1885_CR43
  publication-title: Sci Rep
  doi: 10.1038/s41598-019-42227-5
– volume: 13
  start-page: dmm041947
  year: 2020
  ident: 1885_CR23
  publication-title: Dis Models Mech
  doi: 10.1242/dmm.041947
– volume: 6
  start-page: 114
  year: 2014
  ident: 1885_CR28
  publication-title: Am J Transl Res
– volume: 68
  start-page: 452
  year: 2018
  ident: 1885_CR24
  publication-title: Comp Med
  doi: 10.30802/AALAS-CM-18-000039
– volume: 582
  start-page: 89
  year: 2020
  ident: 1885_CR18
  publication-title: Nature.
  doi: 10.1038/s41586-020-2288-7
– volume: 100
  start-page: 265
  year: 2012
  ident: 1885_CR41
  publication-title: Genomics.
  doi: 10.1016/j.ygeno.2012.07.012
– volume: 330
  start-page: 585
  year: 1994
  ident: 1885_CR86
  publication-title: N Engl J Med
  doi: 10.1056/NEJM199403033300901
– volume: 18
  start-page: 965
  year: 2015
  ident: 1885_CR76
  publication-title: Nat Neurosci
  doi: 10.1038/nn.4030
– volume: 10
  start-page: 310
  year: 2009
  ident: 1885_CR1
  publication-title: Amyotroph Lateral Scler
  doi: 10.3109/17482960802566824
– volume: 352
  start-page: 539
  year: 2016
  ident: 1885_CR69
  publication-title: Science.
  doi: 10.1126/science.aad9378
– volume: 341
  start-page: 1241214
  year: 2013
  ident: 1885_CR83
  publication-title: Science.
  doi: 10.1126/science.1241214
– volume: 132
  start-page: 1815
  year: 2019
  ident: 1885_CR31
  publication-title: Chin Med J
  doi: 10.1097/cm9.0000000000000351
– volume: 9
  start-page: 233
  year: 2011
  ident: 1885_CR36
  publication-title: Nat Rev Microbiol
  doi: 10.1038/nrmicro2536
– volume: 5
  start-page: 23
  year: 2017
  ident: 1885_CR77
  publication-title: Acta Neuropathol Commun.
  doi: 10.1186/s40478-017-0424-x
– volume: 14
  start-page: 475
  year: 2015
  ident: 1885_CR27
  publication-title: Nat Rev Drug Discov
  doi: 10.1038/nrd4609
– volume: 159
  start-page: 344
  year: 2020
  ident: 1885_CR74
  publication-title: Immunology.
  doi: 10.1111/imm.13158
SSID ssj0025774
Score 2.582679
SecondaryResourceType review_article
Snippet Background Much progress has been made in mapping genetic abnormalities linked to amyotrophic lateral sclerosis (ALS), but the majority of cases still present...
Much progress has been made in mapping genetic abnormalities linked to amyotrophic lateral sclerosis (ALS), but the majority of cases still present with no...
Background Much progress has been made in mapping genetic abnormalities linked to amyotrophic lateral sclerosis (ALS), but the majority of cases still present...
Abstract Background Much progress has been made in mapping genetic abnormalities linked to amyotrophic lateral sclerosis (ALS), but the majority of cases still...
SourceID doaj
pubmedcentral
proquest
gale
pubmed
crossref
springer
SourceType Open Website
Open Access Repository
Aggregation Database
Index Database
Enrichment Source
Publisher
StartPage 13
SubjectTerms Abnormalities
ALS
Amyotrophic lateral sclerosis
Animal diseases
Animal models
Antibiotics
Bioavailability
Biodiversity
Biomedicine
Causes of
Development and progression
Digestive system
Disease
Disease modifiers
Gastrointestinal tract
Gene mapping
Genetic abnormalities
Genetic variability
Genetics
Gut microbiota
Health aspects
Host-bacteria relationships
Intestinal microflora
Intestine
Medicine
Medicine & Public Health
Metabolites
Microbial
Microbial activity
Microbial metabolites
Microbiome
Microbiomes
Microbiota
Microbiota (Symbiotic organisms)
Microorganisms
Mutation
Neurodegeneration
Neuroprotection
Neurotoxicity
Neurotransmitters
Nutrients
Pathogenesis
Precision medicine
Review
Sample variance
Therapeutic targets
SummonAdditionalLinks – databaseName: DOAJ Directory of Open Access Journals
  dbid: DOA
  link: http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV1bi9QwFA6yiPgi3q2uGkFQ0bLNpU3i2yguPugiqLA-hSRN3cJMZ5h2lvXfe5Je3K6oL742J7Q51y_05AtCT0OnBfOGpCVTPOVFplKbBW48Rw01hhc8q-JlE-LoSB4fq0_nrvoKPWE9PXCvuAOpoAByJoQtKS9JabMywH6WWeoswJOQfQH1jJupYauVA6oZj8jI4qCFqkZCs21owpIyT9msDEW2_t9z8rmidLFh8sJf01iMDq-jawOKxIv-62-gS765ia58HP6T30LfwPr4-67Dq7onWlr519hgCFi8WRpA2bhuMEA_HDvK_RlAcbyusFn9WHfb9eakdnhpwtnkJW7hBbCEusXPFx8-v7iNvh6--_L2fTpcopA6CK0uzY03lSUlES6nDgyWS-s54xCrubU5LXNJbekq6gHAWpJXviKV4JxJmE-oZ3fQXrNu_D2EKybAqhysahRXnklewf5QFUKIwqpMJYiMOtVuYBgPF10sddxpyEL3dtBgBx3toFmCXk5zNj2_xl-l3wRTTZKBGzs-AI_Rg8fof3lMgh4HQ-v-oOkU4XoBYJXzjFGSoGdRIsQ4LMCZ4agCqCGwZc0k92eSEJtuPjw6kx5yQ6thw5spBmqD5TyZhsPM0O_W-PUuyECepBQqQILu9r43LZoxHkjkYLaYeeVMK_ORpj6JzOFCAvwWeYJejf7767P-rPX7_0PrD9BVGtqBMgKJeR_tddudf4guu9OubrePYvT-BA4cQi4
  priority: 102
  providerName: Directory of Open Access Journals
– databaseName: SpringerLINK Contemporary 1997-Present
  dbid: RSV
  link: http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV3ri9QwEA96ivjF96N6agRBRYvNo03qt1U8_KCHeCrnp5Ck6V1ht122XdH_3kn60J4P0K-bGbqZzOM3ZGaC0ANfacGcJnHBch7zLMljk_jZeJZqqjXPeFKGxybE_r48PMzfDU1h7VjtPl5JBk8dzFpmz1qITMQXzPpCKinTmJ1GZyDcSW-O7w8-TWlWCohmbI_5Ld8sBIVJ_b_6458C0sliyRM3piEQ7V38vy1cQhcG4IkXvaZcRqdcfQWdeztcrV9Fn0Fh8NG2w6uqn820cs-xxmDjeL3UAMxxVWNAizgUobuvgN5xU2K9-tZ0m2Z9XFm81L6deYlb-ADsvGrxo8Wbg8fX0Me9Vx9evo6HdxdiC9bYxal2ujSkIMKm1MIZp9I4zjiYd2pMSotUUlPYkjrAvIakpStJKThnEvgJdew62qmb2t1EuGQCFIGDIuic545JXkJKmWdCiMzkSR4hMh6FssNQcv82xlKF5ERmqpeZApmpIDPFIvRk4ln3Izn-Sv3Cn_BE6cdphx-azZEarFPJHFAWZ0KYgvKCFCYpfG7JEkOtAQwcoXteP1Tfmzo5BbUAfMt5wiiJ0MNA4d0CbMDqobsBxOAHbM0od2eUYM52vjzqoBrcSasgR05yBmKD7dyflj2nL5GrXbP1NOBaKYWgEaEbvcpOm2aM-7lzwC1myjyTynylro7DsHEhAbGLNEJPR5X-8bf-LPVb_0Z-G52nvlYoIeC1d9FOt9m6O-is_dJV7eZuMO_vpsBHiA
  priority: 102
  providerName: Springer Nature
Title The gut microbiome: a key player in the complexity of amyotrophic lateral sclerosis (ALS)
URI https://link.springer.com/article/10.1186/s12916-020-01885-3
https://www.ncbi.nlm.nih.gov/pubmed/33468103
https://www.proquest.com/docview/2490939673
https://www.proquest.com/docview/2479422887
https://pubmed.ncbi.nlm.nih.gov/PMC7816375
https://doaj.org/article/892834377bd24d1db0d042630b2cb192
Volume 19
WOSCitedRecordID wos000609364600001&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D
hasFullText 1
inHoldings 1
isFullTextHit
isPrint
journalDatabaseRights – providerCode: PRVADU
  databaseName: BioMedCentral
  customDbUrl:
  eissn: 1741-7015
  dateEnd: 99991231
  omitProxy: false
  ssIdentifier: ssj0025774
  issn: 1741-7015
  databaseCode: RBZ
  dateStart: 20030101
  isFulltext: true
  titleUrlDefault: https://www.biomedcentral.com/search/
  providerName: BioMedCentral
– providerCode: PRVAON
  databaseName: DOAJ Open Access Journals
  customDbUrl:
  eissn: 1741-7015
  dateEnd: 99991231
  omitProxy: false
  ssIdentifier: ssj0025774
  issn: 1741-7015
  databaseCode: DOA
  dateStart: 20030101
  isFulltext: true
  titleUrlDefault: https://www.doaj.org/
  providerName: Directory of Open Access Journals
– providerCode: PRVHPJ
  databaseName: ROAD: Directory of Open Access Scholarly Resources
  customDbUrl:
  eissn: 1741-7015
  dateEnd: 99991231
  omitProxy: false
  ssIdentifier: ssj0025774
  issn: 1741-7015
  databaseCode: M~E
  dateStart: 20030101
  isFulltext: true
  titleUrlDefault: https://road.issn.org
  providerName: ISSN International Centre
– providerCode: PRVPQU
  databaseName: Health & Medical Collection
  customDbUrl:
  eissn: 1741-7015
  dateEnd: 99991231
  omitProxy: false
  ssIdentifier: ssj0025774
  issn: 1741-7015
  databaseCode: 7X7
  dateStart: 20090101
  isFulltext: true
  titleUrlDefault: https://search.proquest.com/healthcomplete
  providerName: ProQuest
– providerCode: PRVPQU
  databaseName: ProQuest Central
  customDbUrl:
  eissn: 1741-7015
  dateEnd: 99991231
  omitProxy: false
  ssIdentifier: ssj0025774
  issn: 1741-7015
  databaseCode: BENPR
  dateStart: 20090101
  isFulltext: true
  titleUrlDefault: https://www.proquest.com/central
  providerName: ProQuest
– providerCode: PRVPQU
  databaseName: Publicly Available Content Database
  customDbUrl:
  eissn: 1741-7015
  dateEnd: 99991231
  omitProxy: false
  ssIdentifier: ssj0025774
  issn: 1741-7015
  databaseCode: PIMPY
  dateStart: 20090101
  isFulltext: true
  titleUrlDefault: http://search.proquest.com/publiccontent
  providerName: ProQuest
– providerCode: PRVAVX
  databaseName: SpringerLINK Contemporary 1997-Present
  customDbUrl:
  eissn: 1741-7015
  dateEnd: 99991231
  omitProxy: false
  ssIdentifier: ssj0025774
  issn: 1741-7015
  databaseCode: RSV
  dateStart: 20031201
  isFulltext: true
  titleUrlDefault: https://link.springer.com/search?facet-content-type=%22Journal%22
  providerName: Springer Nature
link http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwpR1db9Mw0GIdQrzw_REYxUhIgEa0xHZihxfUoU0gsaraAHVPlp04W6Q2KU2L4N9zdtKMDLEXXiqlPivxfZ99vkPopc20oEaFfkYT5rM4SHwd2Np4KVFEKRazIHfNJvh4LKbTZNJuuNVtWuVGJzpFnVWp3SPfgzABgu8k5vT94rtvu0bZ09W2hcYW2raVytgAbe8fjCfHXcgVgXezuSoj4r0arFtok25tMpYQkU975shV7f9bN_9hnC4nTl46PXVG6fD2_y7nDrrVuqN41PDPXXTNlPfQjaP2wP0-OgU2wmfrFZ4XTcWmuXmHFQbJx4uZAncdFyUGHxK71HTzE3x6XOVYzX9Vq2W1OC9SPFP2kvMM1_ACwEFR49ejzydvHqCvhwdfPnz0224MfgoyuvIjZVSuwyzkaURSoHwktGGUgdBHWkckiwTRWZoTA56wDqPc5GHOGaMC5ofE0IdoUFaleYxwTjmwBwP2UAlLDBUsh0ATkMF5rAEvHgo3RJFpW6rcdsyYSReyiFg2hJRASOkIKamHdrs5i6ZQx5XQ-5bWHaQtsu3-qJZnspVZKRLwvRjlXGeEZWGmg8xGnDTQJNXgGXvoueUU2dxY7VSFHIHXy1hASeihVw7CKgtYQKraOw-ABlt2qwe504MEIU_7wxs2kq2SqeUFD3noRTdsZ9rEudJUawsDCpcQMCUeetQwb7doSpmtRgezeY-te1jpj5TFuStBzgX48Tzy0NuNAFx81r-x_uTqVTxFN4nNGApC0N07aLBars0zdD39sSrq5RBt8Sl3v2LYivnQ7aDA0-TT0eQUno5Pvv0GXMJYbg
linkProvider ProQuest
linkToHtml http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMw1V1bb9MwFLZGh4AX7pfAYEYCAYJoie3EDhJC5TKtWltV2pC2JxMnzhapTUrTAvtT_EaOcxsZYm974LU-TnpOvnNLjs9B6JmptKA6dO2YBsxmvhPYyjG98SISkjBkPnOSctgEH4_FwUEwWUO_mrMwpqyysYmloY7zyLwj34I0AZLvwOf0_fybbaZGma-rzQiNCha7-uQHpGzFu8EneL7PCdn-vP9xx66nCtgRYG1pe6EOE-XGLo88EgEHnlCaUQbg9ZTySOwJouIoIRoiOuV6iU7chDNGBex3iaZw3Uto3dCLHlqfDEaTwzbF8yCaao7mCH-rAG_qmiJfU_wlhGfTjvsrpwT87Qv-cIZnCzXPfK0tneD2jf9NfDfR9Trcxv1KP26hNZ3dRldGdUHBHXQIaoKPVks8S6uOVDP9FocYLBueT0NIR3CaYYiRcVl6r39CzoLzBIezk3y5yOfHaYSnoTnEPcUF3ABknhb4ZX-49-ou-nIhjN1DvSzP9AOEE8oB_gzgHwYs0FSwBBJpED7nvoLnYCG3AYGM6lbsZiLIVJYpmfBlBRwJwJElcCS10Ot2z7xqRHIu9QeDrZbSNBEvf8gXR7K2SVIEEFsyyrmKCYvdWDmxyaipo0ikIPK30KZBpqxO5LamUPYhqmfMocS10IuSwhhDYCAK6zMdIAbTVqxDudGhBCMWdZcb2MraiBbyFLMWetoum52mMDDT-crQgEMhBFylhe5XytIyTSkz3fZgN--oUUcq3ZUsPS5brHMBeQr3LPSmUbjTv_VvqT88n4tNdHVnfzSUw8F49xG6Rkx1lOOCn9pAveVipR-jy9H3ZVosntRmBaOvF62KvwFvhrJa
linkToPdf http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwpV3ri9QwEA96yuEX34_q6UUQVLRcm6RN6rf1sSiey8GpnJ9CkqZ3hd122XZF_3snabdezweIXzczdDOZx2_IzAShR67SgloVhznNWMjSKAt15GbjGaKIUixlUeEfm-CzmTg6yg5OdfH7avfNlWTX0-CmNFXt3jIvOhMX6V4DUSp2xbOuqEqIJKTn0QXmHg1y-frh5yHlSgDdbFplfss3Ckd-av-vvvlUcDpbOHnm9tQHpemV_9_OVXS5B6R40mnQNXTOVtfR9of-yv0G-gKKhI_XLV6U3cymhX2BFQbbx8u5AsCOywoDisS-ON1-A1SP6wKrxfe6XdXLk9LguXJtznPcwAdACmWDn0z2D5_eRJ-mbz6-ehv27zGEBqy0DRNlVaHjPOYmIQbOPhHaMsrA7BOtE5IngujcFMQCFtZxUtgiLjhjVAB_TCy9hbaqurJ3EC4oBwVhoCAqY5mlghWQamYp5zzVWZQFKN4cizT9sHL3ZsZc-qRFpLKTmQSZSS8zSQP0bOBZdqM6_kr90p32QOnGbPsf6tWx7K1WigzQF6Oc65ywPM51lLuck0aaGA3YOEC7Tldk17M6OAs5AdzLWERJHKDHnsK5C9iAUX3XA4jBDd4aUe6MKMHMzXh5o4-ydzONhNw5yiiIDbbzcFh2nK50rrL12tGAyyUEgkmAbnfqO2yaUubm0QE3Hyn2SCrjlao88UPIuQAkz5MAPd-o98-_9Wep3_038l20ffB6Kvffzd7fQ5eIKyeKYnDsO2irXa3tfXTRfG3LZvXAW_0PnnFTUA
openUrl ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=The+gut+microbiome%3A+a+key+player+in+the+complexity+of+amyotrophic+lateral+sclerosis+%28ALS%29&rft.jtitle=BMC+medicine&rft.au=Boddy%2C+Sarah+L&rft.au=Giovannelli%2C+Ilaria&rft.au=Sassani%2C+Matilde&rft.au=Cooper-Knock%2C+Johnathan&rft.date=2021-01-20&rft.eissn=1741-7015&rft.volume=19&rft.issue=1&rft.spage=13&rft_id=info:doi/10.1186%2Fs12916-020-01885-3&rft_id=info%3Apmid%2F33468103&rft.externalDocID=33468103
thumbnail_l http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=1741-7015&client=summon
thumbnail_m http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=1741-7015&client=summon
thumbnail_s http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=1741-7015&client=summon