RNA Sequencing Reveals Small and Variable Contributions of Infectious Agents to Transcriptomes of Postmortem Nervous Tissues From Amyotrophic Lateral Sclerosis, Alzheimer’s Disease and Parkinson’s Disease Subjects, and Increased Expression of Genes From Disease-Activated Microglia
Nervous tissues from both humans with neurodegenerative diseases (NDD) and animals with genetic models of human NDD, such as rare monogenic causes of Amyotrophic Lateral Sclerosis (ALS), Alzheimer's disease (AD), and Parkinson's disease (PD), show activated microglia, suggesting a potentia...
Saved in:
Published in | Frontiers in neuroscience Vol. 13; p. 235 |
---|---|
Main Authors | , , |
Format | Journal Article |
Language | English |
Published |
Switzerland
Frontiers Research Foundation
28.03.2019
Frontiers Media S.A |
Subjects | |
Online Access | Get full text |
Cover
Loading…
Abstract | Nervous tissues from both humans with neurodegenerative diseases (NDD) and animals with genetic models of human NDD, such as rare monogenic causes of Amyotrophic Lateral Sclerosis (ALS), Alzheimer's disease (AD), and Parkinson's disease (PD), show activated microglia, suggesting a potential causal role for inflammation in pathogenesis of NDD. We performed paired-end (PE) RNA sequencing (RNA seq) of total RNA's extracted from frozen sections of cervical spinal cords from ALS and CTL subjects, frontal cortical gray matter ribbons of AD and CTL subjects, and ventral midbrains of PD and CTL subjects. Trimmed PE reads were aligned against the hg38 human transcriptome using Tophat2/Bowtie2 (ALS) or HISAT2 (AD and PD) and quantitated with Cufflinks. PE reads were also aligned using Bowtie2 against genomes from representative species of
and
sp. T6 (parasitic infectious agents),
and
(tick-vector borne agents), and
and
, agents causing chronic gingivitis. Primary aligned reads of each agent in each tissue sample were quantitated with SAMtools. We found small percentages (<0.1%) of transcriptomes aligned with
,
,
, and
genomes and larger percentages aligned with
(0.1-0.2%) and
sp. T6 (1.0-1.1%) genomes. In AD specimens, but in no others, primary aligned transcriptome percentages, although small, approached significance for being greater in AD compared to CTL samples for
(
= 0.067) and
(
= 0.068). Genes' expressions in postmortem tissues of AD and ALS but not PD revealed significant changes among disease-associated microglial (DAM) genes. Infectious agents' transcripts can be detected in RNA seq reads of both NDD and CTL tissues and vary from agent to agent. Expressions of Stage 1 and Stage 2 DAM genes significantly changed, suggesting the presence of Stages 1 and 2 DAM in our NDD tissue samples. |
---|---|
AbstractList | Nervous tissues from both humans with neurodegenerative diseases (NDD) and animals with genetic models of human NDD, such as rare monogenic causes of Amyotrophic Lateral Sclerosis (ALS), Alzheimer’s disease (AD) and Parkinson’s disease (PD), show activated microglia, suggesting a potential causal role for inflammation in NDD. We performed paired-end (PE) RNA sequencing (RNAseq) of total RNA’s extracted from frozen sections of cervical spinal cords from ALS and CTL subjects, frontal cortices of AD and CTL subjects, and ventral midbrains of PD and CTL subjects. Trimmed PE reads were aligned against the hg38 human transcriptome using Tophat2/Bowtie2 and quantitated with Cufflinks. PE reads were also aligned using Bowtie2 against genomes from representative species of Toxoplasma gondii and Trichinella sp T6 (parasitic infectious agents), Babesia microtii and Borrelia burgdorferi (tick-vector borne agents), and Treponema denticola and Porphyromonas gingivalis, agents causing chronic gingivitis. Primary aligned reads of each agent in each tissue sample were quantitated with Samtools. We found small percentages (<0.1%) of transcriptomes aligned with B. microtii, B. burgdorferi, T. denticola and P. gingivalis genomes and larger percentages aligned with T. gondii (0.1-0.2%) and T. sp. 6 (1.0-1.1%) genomes. In AD specimens, but in no others, primary aligned transcriptome percentages, although small, approached significance for being greater in AD compared to CTL samples for B. burgdorferi (p=0.067) and P. gingvalis (p=0.068). Correlation tables of genes’ expressions in all three NDD’s revealed significant correlations among disease-associated microglial (DAM) genes in ALS, AD and PD. Infectious agents’ transcripts can be detected in RNAseq reads of both NDD and CTL tissues and vary from agent to agent. Expressions of Stage 1 and Stage 2 DAM genes significantly correlated with each other, suggesting the presence of Stages 1 and 2 DAM in our NDD tissue samples. (290 words) Nervous tissues from both humans with neurodegenerative diseases (NDD) and animals with genetic models of human NDD, such as rare monogenic causes of Amyotrophic Lateral Sclerosis (ALS), Alzheimer's disease (AD), and Parkinson's disease (PD), show activated microglia, suggesting a potential causal role for inflammation in pathogenesis of NDD. We performed paired-end (PE) RNA sequencing (RNA seq) of total RNA's extracted from frozen sections of cervical spinal cords from ALS and CTL subjects, frontal cortical gray matter ribbons of AD and CTL subjects, and ventral midbrains of PD and CTL subjects. Trimmed PE reads were aligned against the hg38 human transcriptome using Tophat2/Bowtie2 (ALS) or HISAT2 (AD and PD) and quantitated with Cufflinks. PE reads were also aligned using Bowtie2 against genomes from representative species of and sp. T6 (parasitic infectious agents), and (tick-vector borne agents), and and , agents causing chronic gingivitis. Primary aligned reads of each agent in each tissue sample were quantitated with SAMtools. We found small percentages (<0.1%) of transcriptomes aligned with , , , and genomes and larger percentages aligned with (0.1-0.2%) and sp. T6 (1.0-1.1%) genomes. In AD specimens, but in no others, primary aligned transcriptome percentages, although small, approached significance for being greater in AD compared to CTL samples for ( = 0.067) and ( = 0.068). Genes' expressions in postmortem tissues of AD and ALS but not PD revealed significant changes among disease-associated microglial (DAM) genes. Infectious agents' transcripts can be detected in RNA seq reads of both NDD and CTL tissues and vary from agent to agent. Expressions of Stage 1 and Stage 2 DAM genes significantly changed, suggesting the presence of Stages 1 and 2 DAM in our NDD tissue samples. Nervous tissues from both humans with neurodegenerative diseases (NDD) and animals with genetic models of human NDD, such as rare monogenic causes of Amyotrophic Lateral Sclerosis (ALS), Alzheimer's disease (AD), and Parkinson's disease (PD), show activated microglia, suggesting a potential causal role for inflammation in pathogenesis of NDD. We performed paired-end (PE) RNA sequencing (RNA seq) of total RNA's extracted from frozen sections of cervical spinal cords from ALS and CTL subjects, frontal cortical gray matter ribbons of AD and CTL subjects, and ventral midbrains of PD and CTL subjects. Trimmed PE reads were aligned against the hg38 human transcriptome using Tophat2/Bowtie2 (ALS) or HISAT2 (AD and PD) and quantitated with Cufflinks. PE reads were also aligned using Bowtie2 against genomes from representative species of Toxoplasma gondii and Trichinella sp. T6 (parasitic infectious agents), Babesia microti and Borrelia burgdorferi (tick-vector borne agents), and Treponema denticola and Porphyromonas gingivalis, agents causing chronic gingivitis. Primary aligned reads of each agent in each tissue sample were quantitated with SAMtools. We found small percentages (<0.1%) of transcriptomes aligned with B. microti, B. burgdorferi, T. denticola, and P. gingivalis genomes and larger percentages aligned with T. gondii (0.1-0.2%) and Trichinella sp. T6 (1.0-1.1%) genomes. In AD specimens, but in no others, primary aligned transcriptome percentages, although small, approached significance for being greater in AD compared to CTL samples for B. burgdorferi (p = 0.067) and P. gingivalis (p = 0.068). Genes' expressions in postmortem tissues of AD and ALS but not PD revealed significant changes among disease-associated microglial (DAM) genes. Infectious agents' transcripts can be detected in RNA seq reads of both NDD and CTL tissues and vary from agent to agent. Expressions of Stage 1 and Stage 2 DAM genes significantly changed, suggesting the presence of Stages 1 and 2 DAM in our NDD tissue samples.Nervous tissues from both humans with neurodegenerative diseases (NDD) and animals with genetic models of human NDD, such as rare monogenic causes of Amyotrophic Lateral Sclerosis (ALS), Alzheimer's disease (AD), and Parkinson's disease (PD), show activated microglia, suggesting a potential causal role for inflammation in pathogenesis of NDD. We performed paired-end (PE) RNA sequencing (RNA seq) of total RNA's extracted from frozen sections of cervical spinal cords from ALS and CTL subjects, frontal cortical gray matter ribbons of AD and CTL subjects, and ventral midbrains of PD and CTL subjects. Trimmed PE reads were aligned against the hg38 human transcriptome using Tophat2/Bowtie2 (ALS) or HISAT2 (AD and PD) and quantitated with Cufflinks. PE reads were also aligned using Bowtie2 against genomes from representative species of Toxoplasma gondii and Trichinella sp. T6 (parasitic infectious agents), Babesia microti and Borrelia burgdorferi (tick-vector borne agents), and Treponema denticola and Porphyromonas gingivalis, agents causing chronic gingivitis. Primary aligned reads of each agent in each tissue sample were quantitated with SAMtools. We found small percentages (<0.1%) of transcriptomes aligned with B. microti, B. burgdorferi, T. denticola, and P. gingivalis genomes and larger percentages aligned with T. gondii (0.1-0.2%) and Trichinella sp. T6 (1.0-1.1%) genomes. In AD specimens, but in no others, primary aligned transcriptome percentages, although small, approached significance for being greater in AD compared to CTL samples for B. burgdorferi (p = 0.067) and P. gingivalis (p = 0.068). Genes' expressions in postmortem tissues of AD and ALS but not PD revealed significant changes among disease-associated microglial (DAM) genes. Infectious agents' transcripts can be detected in RNA seq reads of both NDD and CTL tissues and vary from agent to agent. Expressions of Stage 1 and Stage 2 DAM genes significantly changed, suggesting the presence of Stages 1 and 2 DAM in our NDD tissue samples. Nervous tissues from both humans with neurodegenerative diseases (NDD) and animals with genetic models of human NDD, such as rare monogenic causes of Amyotrophic Lateral Sclerosis (ALS), Alzheimer’s disease (AD), and Parkinson’s disease (PD), show activated microglia, suggesting a potential causal role for inflammation in pathogenesis of NDD. We performed paired-end (PE) RNA sequencing (RNA seq) of total RNA’s extracted from frozen sections of cervical spinal cords from ALS and CTL subjects, frontal cortical gray matter ribbons of AD and CTL subjects, and ventral midbrains of PD and CTL subjects. Trimmed PE reads were aligned against the hg38 human transcriptome using Tophat2/Bowtie2 (ALS) or HISAT2 (AD and PD) and quantitated with Cufflinks. PE reads were also aligned using Bowtie2 against genomes from representative species of Toxoplasma gondii and Trichinella sp. T6 (parasitic infectious agents), Babesia microti and Borrelia burgdorferi (tick-vector borne agents), and Treponema denticola and Porphyromonas gingivalis, agents causing chronic gingivitis. Primary aligned reads of each agent in each tissue sample were quantitated with SAMtools. We found small percentages (<0.1%) of transcriptomes aligned with B. microti, B. burgdorferi, T. denticola, and P. gingivalis genomes and larger percentages aligned with T. gondii (0.1–0.2%) and Trichinella sp. T6 (1.0–1.1%) genomes. In AD specimens, but in no others, primary aligned transcriptome percentages, although small, approached significance for being greater in AD compared to CTL samples for B. burgdorferi (p = 0.067) and P. gingivalis (p = 0.068). Genes’ expressions in postmortem tissues of AD and ALS but not PD revealed significant changes among disease-associated microglial (DAM) genes. Infectious agents’ transcripts can be detected in RNA seq reads of both NDD and CTL tissues and vary from agent to agent. Expressions of Stage 1 and Stage 2 DAM genes significantly changed, suggesting the presence of Stages 1 and 2 DAM in our NDD tissue samples. Nervous tissues from both humans with neurodegenerative diseases (NDD) and animals with genetic models of human NDD, such as rare monogenic causes of Amyotrophic Lateral Sclerosis (ALS), Alzheimer’s disease (AD), and Parkinson’s disease (PD), show activated microglia, suggesting a potential causal role for inflammation in pathogenesis of NDD. We performed paired-end (PE) RNA sequencing (RNA seq) of total RNA’s extracted from frozen sections of cervical spinal cords from ALS and CTL subjects, frontal cortical gray matter ribbons of AD and CTL subjects, and ventral midbrains of PD and CTL subjects. Trimmed PE reads were aligned against the hg38 human transcriptome using Tophat2/Bowtie2 (ALS) or HISAT2 (AD and PD) and quantitated with Cufflinks. PE reads were also aligned using Bowtie2 against genomes from representative species of Toxoplasma gondii and Trichinella sp. T6 (parasitic infectious agents), Babesia microti and Borrelia burgdorferi (tick-vector borne agents), and Treponema denticola and Porphyromonas gingivalis , agents causing chronic gingivitis. Primary aligned reads of each agent in each tissue sample were quantitated with SAMtools. We found small percentages (<0.1%) of transcriptomes aligned with B. microti , B. burgdorferi , T. denticola , and P. gingivalis genomes and larger percentages aligned with T. gondii (0.1–0.2%) and Trichinella sp. T6 (1.0–1.1%) genomes. In AD specimens, but in no others, primary aligned transcriptome percentages, although small, approached significance for being greater in AD compared to CTL samples for B. burgdorferi ( p = 0.067) and P. gingivalis ( p = 0.068). Genes’ expressions in postmortem tissues of AD and ALS but not PD revealed significant changes among disease-associated microglial (DAM) genes. Infectious agents’ transcripts can be detected in RNA seq reads of both NDD and CTL tissues and vary from agent to agent. Expressions of Stage 1 and Stage 2 DAM genes significantly changed, suggesting the presence of Stages 1 and 2 DAM in our NDD tissue samples. |
Author | Brohawn, David G. Keeney, Paula M. Bennett, James P. |
AuthorAffiliation | 1 Neurodegeneration Therapeutics, Inc. , Charlottesville, VA , United States 2 Parkinson’s and Movement Disorders Center, Virginia Commonwealth University , Richmond, VA , United States 3 Department of Medical Genetics, Virginia Commonwealth University , Richmond, VA , United States |
AuthorAffiliation_xml | – name: 1 Neurodegeneration Therapeutics, Inc. , Charlottesville, VA , United States – name: 2 Parkinson’s and Movement Disorders Center, Virginia Commonwealth University , Richmond, VA , United States – name: 3 Department of Medical Genetics, Virginia Commonwealth University , Richmond, VA , United States |
Author_xml | – sequence: 1 givenname: James P. surname: Bennett fullname: Bennett, James P. – sequence: 2 givenname: Paula M. surname: Keeney fullname: Keeney, Paula M. – sequence: 3 givenname: David G. surname: Brohawn fullname: Brohawn, David G. |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/30983949$$D View this record in MEDLINE/PubMed |
BookMark | eNp1Uk1v1DAQDaiIfsCdC8gSFw5scex8XpCipS0rlVJ1C-JmeZ3J1ktiL7azopz4G_w9fgmT3W3VVuIUx_Pm-c2btx_tGGsgil7E9JDzonzXGG38IaNxeUgp4-njaC_OMjZKUv5t5855N9r3fkFpxoqEPY12OS0LXibl3qOXF2cVmcKPHozSZk4uYAWy9WTaybYl0tTkq3RazlogY2uC07M-aGs8sQ2ZmAYU_vWeVHMwwZNgyaWTxiunl8F2sIadWx866wJ05AzcaoBfau97rB4725Gqu7bB2eWVVuRUBnCyJVPVgrNe-7ekan9dge7A_f39x5MP2oP0sFZ2Lt13nN-ae5VpP1ugLOwcMBOj3HBdk6OfSwfeo_hB1AmYm_e3jaMKZ1nh-zX5pJWz81bLZ9GTBt2A59vvQfTl-Ohy_HF0-vlkMq5ORyopaRjFtEhzXja0yGihOM3qOm14w-uCMZUwmkKRZzSNm4zFmcoTReksKeo8LTkUTVrzg2iy4a2tXIil051018JKLdYX1s2FdEGjKSJnMS9lzCkgR5KWJc-VLIoZZVTWuFPker_hWvazDmqFi0FH75Herxh9JeZ2JbIkybOYIcGbLYGzmAsfRKe9graVBnB5grGYUppSliP09QPowvbOoFWCoQ1pwvJ0UPTqrqJbKTcpRADdANB27x00t5CYiiHoYh10MQRdrIOOLdmDFqWDHKKJM-n2_43_ANvvCnA |
CitedBy_id | crossref_primary_10_1080_1040841X_2022_2163613 crossref_primary_10_1016_j_jchemneu_2023_102236 crossref_primary_10_1016_j_mito_2020_05_012 crossref_primary_10_1186_s13195_020_00654_x crossref_primary_10_1016_j_bbi_2024_09_011 crossref_primary_10_1186_s12974_020_01822_4 crossref_primary_10_1038_s41598_020_67691_2 crossref_primary_10_3390_pharmaceutics17020141 crossref_primary_10_1016_j_jneuroim_2020_577185 crossref_primary_10_1111_prd_12429 crossref_primary_10_1016_j_aggp_2024_100061 crossref_primary_10_3390_ijms21072495 crossref_primary_10_1038_s41598_020_59364_x crossref_primary_10_3390_brainsci14040358 crossref_primary_10_1007_s00401_021_02401_4 crossref_primary_10_2147_NDT_S264910 crossref_primary_10_3390_microorganisms9061301 crossref_primary_10_3389_fgene_2021_585556 crossref_primary_10_3390_biom13060922 crossref_primary_10_1080_20002297_2020_1820834 crossref_primary_10_1016_j_tig_2019_12_002 crossref_primary_10_3389_fnagi_2022_1052805 crossref_primary_10_1128_msphere_00826_24 crossref_primary_10_3390_ijms252011168 crossref_primary_10_1016_j_chom_2020_06_008 crossref_primary_10_1093_jnen_nlac110 crossref_primary_10_1126_sciadv_abd1707 crossref_primary_10_4081_oncol_2020_476 crossref_primary_10_1093_g3journal_jkab141 |
Cites_doi | 10.1007/s12035-017-0532-4 10.4103/sni.sni_441_16 10.1007/s00702-017-1745-4 10.3389/fnagi.2017.00129 10.3389/fnins.2017.00680 10.1016/j.ejmech.2017.09.001 10.1016/j.cell.2017.05.018 10.1038/nmeth.3317 10.1146/annurev-physiol-022516-034406 10.1080/00207454.2016.1264072 10.1016/j.neulet.2017.06.050 10.1186/s13024-017-0197-5 10.3390/ijms18050993 10.1002/glia.23154 10.1371/journal.pone.0160520 10.1002/mds.27037 10.1146/annurev-immunol-051116-052358 10.1515/bmc-2016-0029 10.1016/j.jalz.2016.02.010 10.1146/annurev-med-050715-104343 10.1016/j.freeradbiomed.2017.08.006 10.1186/s12974-016-0620-9 10.3389/fnagi.2017.00194 10.1016/j.ynstr.2018.05.003 10.3892/mmr.2016.4948 10.1155/2016/7205747 10.1007/s40520-016-0637-z 10.2174/1874205X01812010050 10.3389/fnagi.2017.00094 10.3389/fncel.2018.00114 10.1016/j.coph.2015.10.001 10.1016/j.immuni.2017.06.007 10.1016/j.neuint.2018.07.003 10.3389/fnagi.2017.00193 10.1016/j.bcp.2016.08.001 10.1016/j.brainres.2017.05.010 10.1016/j.cell.2018.05.003 10.3390/ijms18030561 10.3233/BPL-140001 10.1007/s12035-016-0297-1 10.1016/j.exger.2017.01.027 10.1016/j.jns.2017.03.031 10.15761/jsin.1000178 10.3389/fnagi.2017.00128 10.1021/acschemneuro.5b00313 10.2174/1567205013666151116141217 10.1007/s12035-016-0245-0 10.1016/j.bbi.2015.07.003 10.1016/j.jmb.2017.04.004 10.1016/j.bbamcr.2016.03.018 10.3390/ijms18030504 10.1080/01616412.2016.1251711 10.1111/bpa.12352 10.1124/mol.117.109512 10.3390/ijms18040769 10.1021/acschemneuro.7b00176 10.18632/oncotarget.23106 10.3233/JAD-179929 10.3390/ijms18030598 10.1007/s00702-017-1795-7 10.15761/JSCRM.1000124 10.3233/JAD-179925 10.1016/j.pneurobio.2016.04.006 10.1089/ars.2017.7099 10.1172/JCI90607 10.1126/science.aag2590 10.1016/j.neuropharm.2015.09.019 10.17420/ap6304.111 10.1002/glia.22988 |
ContentType | Journal Article |
Copyright | 2019. 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 © 2019 Bennett, Keeney and Brohawn. 2019 Bennett, Keeney and Brohawn |
Copyright_xml | – notice: 2019. 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. – notice: Copyright © 2019 Bennett, Keeney and Brohawn. 2019 Bennett, Keeney and Brohawn |
DBID | AAYXX CITATION NPM 3V. 7XB 88I 8FE 8FH 8FK ABUWG AFKRA AZQEC BBNVY BENPR BHPHI CCPQU DWQXO GNUQQ HCIFZ LK8 M2P M7P PHGZM PHGZT PIMPY PKEHL PQEST PQGLB PQQKQ PQUKI PRINS Q9U 7X8 5PM DOA |
DOI | 10.3389/fnins.2019.00235 |
DatabaseName | CrossRef PubMed ProQuest Central (Corporate) ProQuest Central (purchase pre-March 2016) Science Database (Alumni Edition) ProQuest SciTech Collection ProQuest Natural Science Collection ProQuest Central (Alumni) (purchase pre-March 2016) ProQuest Central (Alumni) ProQuest Central UK/Ireland ProQuest Central Essentials - QC Biological Science Collection ProQuest Central Natural Science Collection ProQuest One Community College ProQuest Central ProQuest Central Student SciTech Premium Collection ProQuest Biological Science Collection Science Database Biological Science Database ProQuest Central Premium ProQuest One Academic (New) Publicly Available Content Database ProQuest One Academic Middle East (New) ProQuest One Academic Eastern Edition (DO NOT USE) ProQuest One Applied & Life Sciences ProQuest One Academic ProQuest One Academic UKI Edition ProQuest Central China ProQuest Central Basic MEDLINE - Academic PubMed Central (Full Participant titles) DOAJ Directory of Open Access Journals |
DatabaseTitle | CrossRef PubMed Publicly Available Content Database ProQuest Central Student ProQuest One Academic Middle East (New) ProQuest Central Essentials ProQuest Central (Alumni Edition) SciTech Premium Collection ProQuest One Community College ProQuest Natural Science Collection ProQuest Central China ProQuest Central ProQuest One Applied & Life Sciences Natural Science Collection ProQuest Central Korea Biological Science Collection ProQuest Central (New) ProQuest Science Journals (Alumni Edition) ProQuest Biological Science Collection ProQuest Central Basic ProQuest Science Journals ProQuest One Academic Eastern Edition Biological Science Database ProQuest SciTech Collection 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 Directory of Open Access Journals url: https://www.doaj.org/ sourceTypes: Open Website – sequence: 2 dbid: NPM name: PubMed url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 3 dbid: BENPR name: ProQuest Central url: https://www.proquest.com/central sourceTypes: Aggregation Database |
DeliveryMethod | fulltext_linktorsrc |
Discipline | Anatomy & Physiology |
EISSN | 1662-453X |
ExternalDocumentID | oai_doaj_org_article_72139a130e0b4459937ca88b020ad394 PMC6447612 30983949 10_3389_fnins_2019_00235 |
Genre | Journal Article |
GeographicLocations | United States--US Virginia |
GeographicLocations_xml | – name: United States--US – name: Virginia |
GroupedDBID | --- 29H 2WC 53G 5GY 5VS 88I 8FE 8FH 9T4 AAFWJ AAYXX ABUWG ACGFO ACGFS ACXDI ADRAZ AEGXH AENEX AFKRA AFPKN AIAGR ALMA_UNASSIGNED_HOLDINGS AZQEC BBNVY BENPR BHPHI BPHCQ CCPQU CITATION CS3 DIK DU5 DWQXO E3Z EBS EJD EMOBN F5P FRP GNUQQ GROUPED_DOAJ GX1 HCIFZ HYE KQ8 LK8 M2P M48 M7P O5R O5S OK1 OVT P2P PGMZT PHGZM PHGZT PIMPY PQQKQ PROAC RNS RPM W2D C1A NPM 3V. 7XB 8FK PKEHL PQEST PQGLB PQUKI PRINS Q9U 7X8 5PM PUEGO |
ID | FETCH-LOGICAL-c490t-1085739f08608c306dd5f3f3d822c4205e876051f6216c74c00b48d7593e8f5d3 |
IEDL.DBID | M48 |
ISSN | 1662-453X 1662-4548 |
IngestDate | Wed Aug 27 01:30:08 EDT 2025 Thu Aug 21 18:22:57 EDT 2025 Fri Jul 11 11:21:53 EDT 2025 Fri Jul 25 11:44:59 EDT 2025 Thu Apr 03 07:03:49 EDT 2025 Tue Jul 01 01:01:33 EDT 2025 Thu Apr 24 23:03:30 EDT 2025 |
IsDoiOpenAccess | true |
IsOpenAccess | true |
IsPeerReviewed | true |
IsScholarly | true |
Keywords | ALS neurodegeneration Alzheimer’s disease microglia Parkinson’s disease gene expression |
Language | English |
License | This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
LinkModel | DirectLink |
MergedId | FETCHMERGED-LOGICAL-c490t-1085739f08608c306dd5f3f3d822c4205e876051f6216c74c00b48d7593e8f5d3 |
Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 Present address: David G. Brohawn, UCLA Technology Center for Genomics & Bioinformatics, Department of Pathology and Laboratory Medicine, Los Angeles, CA, United States This article was submitted to Neurodegeneration, a section of the journal Frontiers in Neuroscience Edited by: Vincenzo La Bella, University of Palermo, Italy Reviewed by: Isabella Russo, Università degli Studi di Brescia, Italy; Patrizia Longone, Fondazione Santa Lucia (IRCCS), Italy |
OpenAccessLink | https://doaj.org/article/72139a130e0b4459937ca88b020ad394 |
PMID | 30983949 |
PQID | 2306542754 |
PQPubID | 4424402 |
ParticipantIDs | doaj_primary_oai_doaj_org_article_72139a130e0b4459937ca88b020ad394 pubmedcentral_primary_oai_pubmedcentral_nih_gov_6447612 proquest_miscellaneous_2210005027 proquest_journals_2306542754 pubmed_primary_30983949 crossref_primary_10_3389_fnins_2019_00235 crossref_citationtrail_10_3389_fnins_2019_00235 |
ProviderPackageCode | CITATION AAYXX |
PublicationCentury | 2000 |
PublicationDate | 2019-03-28 |
PublicationDateYYYYMMDD | 2019-03-28 |
PublicationDate_xml | – month: 03 year: 2019 text: 2019-03-28 day: 28 |
PublicationDecade | 2010 |
PublicationPlace | Switzerland |
PublicationPlace_xml | – name: Switzerland – name: Lausanne |
PublicationTitle | Frontiers in neuroscience |
PublicationTitleAlternate | Front Neurosci |
PublicationYear | 2019 |
Publisher | Frontiers Research Foundation Frontiers Media S.A |
Publisher_xml | – name: Frontiers Research Foundation – name: Frontiers Media S.A |
References | Deczkowska (B25) 2018; 173 Du (B26) 2017; 54 Toledano (B63) 2016; 13 Wolf (B69) 2017; 79 Plaza-Zabala (B47) 2017; 18 Yan (B70) 2017; 92 Guerriero (B29) 2017; 29 Tse (B65) 2017; 8 Bolos (B13) 2017; 8 Chen (B19) 2016; 26 Aguilera (B1) 2018; 28 Herz (B31) 2017; 46 Calsolaro (B16) 2016; 12 Bennett (B8) 2016; 117 Ransohoff (B49) 2016; 353 Spagnuolo (B58) 2018; 153 Casas (B17) 2016; 1 Keren-Shaul (B35) 2017; 169 Colonna (B23) 2017; 35 Joers (B34) 2017; 155 Selles (B53) 2018; 64 Sorce (B57) 2017; 112 Lall (B42) 2017; 127 Lannes (B43) 2017; 8 Puentes (B48) 2016; 26 Islam (B32) 2017; 39 Labandeira-Garcia (B39) 2017; 9 Brohawn (B14) 2018; 2 Maccioni (B44) 2018; 12 Sochocka (B55) 2017; 54 Rothaug (B51) 2016 Spittau (B59) 2017; 9 Clayton (B21) 2017; 11 Ulrich (B66) 2016; 7 Labzin (B40) 2018; 69 Bisht (B10) 2018; 9 Taylor (B61) 2018; 125 Yang (B71) 2017; 9 Bennett (B7) 2017; 3 Brohawn (B15) 2016; 11 Dzikowiec (B27) 2017; 63 Koellhoffer (B38) 2017; 18 Crisafulli (B24) 2018; 55 Chen (B20) 2016; 13 Cerami (B18) 2017; 18 Su (B60) 2016; 52 Blank (B11) 2017; 65 Kober (B37) 2017; 429 Baufeld (B5) 2018; 125 Blaylock (B12) 2017; 8 van Horssen (B67) 2017 Au (B3) 2017; 9 Nissen (B46) 2017; 18 Trias (B64) 2016; 13 Han (B30) 2017; 127 Bagyinszky (B4) 2017; 376 Solleiro-Villavicencio (B56) 2018; 12 Ladd (B41) 2017; 1667 Roser (B50) 2017; 9 Beamer (B6) 2016; 104 Kim (B36) 2015; 12 Wes (B68) 2016; 64 Bickford (B9) 2017; 94 Collier (B22) 2017; 32 Asiimwe (B2) 2016; 2016 Jay (B33) 2017; 12 Thompson (B62) 2017; 18 Edison (B28) 2018; 64 Niranjan (B45) 2018; 120 |
References_xml | – volume: 55 start-page: 2789 year: 2018 ident: B24 article-title: Therapeutic strategies under development targeting inflammatory mechanisms in amyotrophic lateral sclerosis. publication-title: Mol. Neurobiol. doi: 10.1007/s12035-017-0532-4 – volume: 8 year: 2017 ident: B12 article-title: Parkinson’s disease: microglial/macrophage-induced immunoexcitotoxicity as a central mechanism of neurodegeneration. publication-title: Surg. Neurol. Int. doi: 10.4103/sni.sni_441_16 – volume: 125 start-page: 797 year: 2018 ident: B61 article-title: Type-I interferon pathway in neuroinflammation and neurodegeneration: focus on alzheimer’s disease. publication-title: J. Neural Transm. doi: 10.1007/s00702-017-1745-4 – volume: 9 year: 2017 ident: B39 article-title: Brain renin-angiotensin system and microglial polarization: implications for aging and neurodegeneration. publication-title: Front. Aging Neurosci. doi: 10.3389/fnagi.2017.00129 – volume: 11 year: 2017 ident: B21 article-title: Alzheimer’s disease: the role of microglia in brain homeostasis and proteopathy. publication-title: Front. Neurosci. doi: 10.3389/fnins.2017.00680 – volume: 153 start-page: 105 year: 2018 ident: B58 article-title: Anti-inflammatory effects of flavonoids in neurodegenerative disorders. publication-title: Eur. J. Med. Chem. doi: 10.1016/j.ejmech.2017.09.001 – volume: 169 year: 2017 ident: B35 article-title: A unique microglia type associated with restricting development of alzheimer’s disease. publication-title: Cell doi: 10.1016/j.cell.2017.05.018 – volume: 12 start-page: 357 year: 2015 ident: B36 article-title: HISAT: a fast spliced aligner with low memory requirements. publication-title: Nat. Methods doi: 10.1038/nmeth.3317 – volume: 79 start-page: 619 year: 2017 ident: B69 article-title: Microglia in physiology and disease. publication-title: Annu. Rev. Physiol. doi: 10.1146/annurev-physiol-022516-034406 – volume: 127 start-page: 368 year: 2017 ident: B30 article-title: Contributions of triggering-receptor-expressed-on-myeloid-cells-2 to neurological diseases. publication-title: Int. J. Neurosci. doi: 10.1080/00207454.2016.1264072 – year: 2017 ident: B67 article-title: Inflammation and mitochondrial dysfunction: a vicious circle in neurodegenerative disorders? publication-title: Neurosci. Lett doi: 10.1016/j.neulet.2017.06.050 – volume: 12 year: 2017 ident: B33 article-title: TREM2 in neurodegenerative diseases. publication-title: Mol. Neurodegener. doi: 10.1186/s13024-017-0197-5 – volume: 18 year: 2017 ident: B18 article-title: Molecular imaging of neuroinflammation in neurodegenerative dementias: the role of in vivo PET imaging. publication-title: Int. J. Mol. Sci. doi: 10.3390/ijms18050993 – volume: 65 start-page: 1397 year: 2017 ident: B11 article-title: Type I interferon pathway in CNS homeostasis and neurological disorders. publication-title: Glia doi: 10.1002/glia.23154 – volume: 11 year: 2016 ident: B15 article-title: RNAseq analyses identify tumor necrosis factor-mediated inflammation as a major abnormality in ALS spinal cord. publication-title: PLoS One doi: 10.1371/journal.pone.0160520 – volume: 32 start-page: 983 year: 2017 ident: B22 article-title: Aging and parkinson’s disease: different sides of the same coin? publication-title: Mov. Disord. doi: 10.1002/mds.27037 – volume: 35 start-page: 441 year: 2017 ident: B23 article-title: Microglia function in the central nervous system during health and neurodegeneration. publication-title: Annu. Rev. Immunol. doi: 10.1146/annurev-immunol-051116-052358 – volume: 8 start-page: 37 year: 2017 ident: B13 article-title: Alzheimer’s disease as an inflammatory disease. publication-title: Biomol. Concepts doi: 10.1515/bmc-2016-0029 – volume: 12 start-page: 719 year: 2016 ident: B16 article-title: Neuroinflammation in alzheimer’s disease: current evidence and future directions. publication-title: Alzheimers Dement doi: 10.1016/j.jalz.2016.02.010 – volume: 69 start-page: 437 year: 2018 ident: B40 article-title: Innate immunity and neurodegeneration. publication-title: Annu. Rev. Med. doi: 10.1146/annurev-med-050715-104343 – volume: 112 start-page: 387 year: 2017 ident: B57 article-title: NADPH oxidases as drug targets and biomarkers in neurodegenerative diseases: what is the evidence? publication-title: Free Radic Biol. Med. doi: 10.1016/j.freeradbiomed.2017.08.006 – volume: 13 year: 2016 ident: B64 article-title: Post-paralysis tyrosine kinase inhibition with masitinib abrogates neuroinflammation and slows disease progression in inherited amyotrophic lateral sclerosis. publication-title: J. Neuroinflamm. doi: 10.1186/s12974-016-0620-9 – volume: 9 year: 2017 ident: B59 article-title: Aging microglia-phenotypes, functions and implications for age-related neurodegenerative diseases. publication-title: Front. Aging Neurosci. doi: 10.3389/fnagi.2017.00194 – volume: 9 start-page: 9 year: 2018 ident: B10 article-title: Chronic stress as a risk factor for alzheimer’s disease: roles of microglia-mediated synaptic remodeling, inflammation, and oxidative stress. publication-title: Neurobiol. Stress doi: 10.1016/j.ynstr.2018.05.003 – volume: 13 start-page: 3391 year: 2016 ident: B20 article-title: Role of neuroinflammation in neurodegenerative diseases (Review). publication-title: Mol. Med. Rep. doi: 10.3892/mmr.2016.4948 – volume: 2016 year: 2016 ident: B2 article-title: Nitric oxide: exploring the contextual link with alzheimer’s disease. publication-title: Oxid. Med. Cell. Longev. doi: 10.1155/2016/7205747 – volume: 29 start-page: 821 year: 2017 ident: B29 article-title: Neuroinflammation, immune system and alzheimer disease: searching for the missing link. publication-title: Aging Clin. Exp. Res. doi: 10.1007/s40520-016-0637-z – volume: 12 start-page: 50 year: 2018 ident: B44 article-title: Alzheimer s disease in the perspective of neuroimmunology. publication-title: Open Neurol. J. doi: 10.2174/1874205X01812010050 – volume: 9 year: 2017 ident: B50 article-title: Modulation of microglial activity by Rho-Kinase (ROCK) inhibition as therapeutic strategy in parkinson’s disease and amyotrophic lateral sclerosis. publication-title: Front. Aging Neurosci. doi: 10.3389/fnagi.2017.00094 – volume: 12 year: 2018 ident: B56 article-title: Effect of chronic oxidative stress on neuroinflammatory response mediated by CD4(+)T cells in neurodegenerative diseases. publication-title: Front. Cell Neurosci. doi: 10.3389/fncel.2018.00114 – volume: 26 start-page: 54 year: 2016 ident: B19 article-title: Critical role of the Mac1/NOX2 pathway in mediating reactive microgliosis-generated chronic neuroinflammation and progressive neurodegeneration. publication-title: Curr. Opin. Pharmacol. doi: 10.1016/j.coph.2015.10.001 – volume: 46 start-page: 943 year: 2017 ident: B31 article-title: Myeloid cells in the central nervous system. publication-title: Immunity doi: 10.1016/j.immuni.2017.06.007 – volume: 120 start-page: 13 year: 2018 ident: B45 article-title: Recent advances in the mechanisms of neuroinflammation and their roles in neurodegeneration. publication-title: Neurochem. Int. doi: 10.1016/j.neuint.2018.07.003 – volume: 9 year: 2017 ident: B71 article-title: Microglial activation in the pathogenesis of huntington’s disease. publication-title: Front. Aging Neurosci. doi: 10.3389/fnagi.2017.00193 – volume: 117 start-page: 68 year: 2016 ident: B8 article-title: Pharmacological properties of microneurotrophin drugs developed for treatment of amyotrophic lateral sclerosis. publication-title: Biochem. Pharmacol. doi: 10.1016/j.bcp.2016.08.001 – volume: 1667 start-page: 74 year: 2017 ident: B41 article-title: RNA-seq analyses reveal that cervical spinal cords and anterior motor neurons from amyotrophic lateral sclerosis subjects show reduced expression of mitochondrial DNA-encoded respiratory genes, and rhTFAM may correct this respiratory deficiency. publication-title: Brain Res. doi: 10.1016/j.brainres.2017.05.010 – volume: 173 start-page: 1073 year: 2018 ident: B25 article-title: Disease-associated microglia: a universal immune sensor of neurodegeneration. publication-title: Cell doi: 10.1016/j.cell.2018.05.003 – volume: 18 year: 2017 ident: B46 article-title: Microglial function across the spectrum of age and gender. publication-title: Int. J. Mol. Sci. doi: 10.3390/ijms18030561 – volume: 1 start-page: 159 year: 2016 ident: B17 article-title: Synaptic failure: focus in an integrative view of ALS. publication-title: Brain Plast doi: 10.3233/BPL-140001 – volume: 54 start-page: 8071 year: 2017 ident: B55 article-title: Inflammatory response in the CNS: friend or foe? publication-title: Mol. Neurobiol. doi: 10.1007/s12035-016-0297-1 – volume: 94 start-page: 4 year: 2017 ident: B9 article-title: Aging leads to altered microglial function that reduces brain resiliency increasing vulnerability to neurodegenerative diseases. publication-title: Exp. Gerontol. doi: 10.1016/j.exger.2017.01.027 – volume: 376 start-page: 242 year: 2017 ident: B4 article-title: Role of inflammatory molecules in the alzheimer’s disease progression and diagnosis. publication-title: J. Neurol. Sci. doi: 10.1016/j.jns.2017.03.031 – volume: 3 start-page: 1 year: 2017 ident: B7 article-title: Micro RNA’s (mirna’s) may help explain expression of multiple genes in alzheimer’s frontal cortex. publication-title: Journal of Systems and Integrative Neuroscience doi: 10.15761/jsin.1000178 – volume: 9 year: 2017 ident: B3 article-title: Recent advances in the study of bipolar/rod-shaped microglia and their roles in neurodegeneration. publication-title: Front. Aging Neurosci. doi: 10.3389/fnagi.2017.00128 – volume: 7 start-page: 420 year: 2016 ident: B66 article-title: TREM2 function in alzheimer’s disease and neurodegeneration. publication-title: ACS Chem. Neurosci. doi: 10.1021/acschemneuro.5b00313 – volume: 13 start-page: 321 year: 2016 ident: B63 article-title: Brain local and regional neuroglial alterations in alzheimer’s disease: cell types, responses and implications. publication-title: Curr. Alzheimer Res. doi: 10.2174/1567205013666151116141217 – volume: 54 start-page: 7567 year: 2017 ident: B26 article-title: Role of microglia in neurological disorders and their potentials as a therapeutic target. publication-title: Mol. Neurobiol. doi: 10.1007/s12035-016-0245-0 – volume: 52 start-page: 1 year: 2016 ident: B60 article-title: MicroRNAs mediating CNS inflammation: small regulators with powerful potential. publication-title: Brain Behav. Immun. doi: 10.1016/j.bbi.2015.07.003 – volume: 429 start-page: 1607 year: 2017 ident: B37 article-title: TREM2-ligand interactions in health and disease. publication-title: J. Mol. Biol. doi: 10.1016/j.jmb.2017.04.004 – start-page: 1218 year: 2016 ident: B51 article-title: The role of interleukin-6 signaling in nervous tissue. publication-title: Biochim. Biophys. Acta doi: 10.1016/j.bbamcr.2016.03.018 – volume: 18 year: 2017 ident: B62 article-title: The diverse roles of microglia in the neurodegenerative aspects of Central Nervous System (CNS) autoimmunity. publication-title: Int. J. Mol. Sci. doi: 10.3390/ijms18030504 – volume: 39 start-page: 73 year: 2017 ident: B32 article-title: Oxidative stress and mitochondrial dysfunction-linked neurodegenerative disorders. publication-title: Neurol. Res. doi: 10.1080/01616412.2016.1251711 – volume: 26 start-page: 248 year: 2016 ident: B48 article-title: Non-neuronal cells in ALS: role of glial, immune cells and blood-CNS barriers. publication-title: Brain Pathol. doi: 10.1111/bpa.12352 – volume: 92 start-page: 640 year: 2017 ident: B70 article-title: Activation of AMPK/mTORC1-mediated autophagy by metformin reverses Clk1 deficiency-sensitized dopaminergic neuronal death. publication-title: Mol. Pharmacol. doi: 10.1124/mol.117.109512 – volume: 18 year: 2017 ident: B38 article-title: Old maids: aging and its impact on microglia function. publication-title: Int. J. Mol. Sci. doi: 10.3390/ijms18040769 – volume: 8 start-page: 1438 year: 2017 ident: B65 article-title: Gut microbiota, nitric oxide, and microglia as prerequisites for neurodegenerative disorders. publication-title: ACS Chem. Neurosci. doi: 10.1021/acschemneuro.7b00176 – volume: 8 start-page: 114393 year: 2017 ident: B43 article-title: Microglia at center stage: a comprehensive review about the versatile and unique residential macrophages of the central nervous system. publication-title: Oncotarget doi: 10.18632/oncotarget.23106 – volume: 64 start-page: S339 year: 2018 ident: B28 article-title: Role of neuroinflammation in the trajectory of alzheimer’s disease and in vivo quantification using PET. publication-title: J. Alzheimers Dis. doi: 10.3233/JAD-179929 – volume: 18 year: 2017 ident: B47 article-title: Autophagy and microglia: novel partners in neurodegeneration and aging. publication-title: Int. J. Mol. Sci. doi: 10.3390/ijms18030598 – volume: 125 start-page: 809 year: 2018 ident: B5 article-title: Differential contribution of microglia and monocytes in neurodegenerative diseases. publication-title: J. Neural Transm. doi: 10.1007/s00702-017-1795-7 – volume: 2 start-page: 1 year: 2018 ident: B14 article-title: < Neuralized human embryonic or induced pluripotential stem cell-derived motor neurons are genetically different from those isolated from human adult cervical spinal cord. pdf >. publication-title: J. Stem Cell Res. Med. doi: 10.15761/JSCRM.1000124 – volume: 64 start-page: S313 year: 2018 ident: B53 article-title: Brain inflammation connects cognitive and non-cognitive symptoms in alzheimer’s disease. publication-title: J. Alzheimers Dis. doi: 10.3233/JAD-179925 – volume: 155 start-page: 57 year: 2017 ident: B34 article-title: Microglial phenotypes in Parkinson’s disease and animal models of the disease. publication-title: Prog. Neurobiol. doi: 10.1016/j.pneurobio.2016.04.006 – volume: 28 start-page: 1626 year: 2018 ident: B1 article-title: Redox signaling, neuroinflammation, and neurodegeneration. publication-title: Antioxid. Redox Signal. doi: 10.1089/ars.2017.7099 – volume: 127 start-page: 3250 year: 2017 ident: B42 article-title: Microglia and C9orf72 in neuroinflammation and ALS and frontotemporal dementia. publication-title: J. Clin. Invest. doi: 10.1172/JCI90607 – volume: 353 start-page: 777 year: 2016 ident: B49 article-title: How neuroinflammation contributes to neurodegeneration. publication-title: Science doi: 10.1126/science.aag2590 – volume: 104 start-page: 94 year: 2016 ident: B6 article-title: Purinergic mechanisms in neuroinflammation: an update from molecules to behavior. publication-title: Neuropharmacology doi: 10.1016/j.neuropharm.2015.09.019 – volume: 63 start-page: 243 year: 2017 ident: B27 article-title: Neuroinvasions caused by parasites. publication-title: Ann. Parasitol. doi: 10.17420/ap6304.111 – volume: 64 start-page: 1710 year: 2016 ident: B68 article-title: Targeting microglia for the treatment of alzheimer’s disease. publication-title: Glia doi: 10.1002/glia.22988 |
SSID | ssj0062842 |
Score | 2.3396187 |
Snippet | Nervous tissues from both humans with neurodegenerative diseases (NDD) and animals with genetic models of human NDD, such as rare monogenic causes of... |
SourceID | doaj pubmedcentral proquest pubmed crossref |
SourceType | Open Website Open Access Repository Aggregation Database Index Database Enrichment Source |
StartPage | 235 |
SubjectTerms | Aging ALS Alzheimer's disease Amyotrophic lateral sclerosis Animal models Cytotoxicity Disease Gene expression Genes Genomes Gingivitis Lymphocytes T Microglia Movement disorders Neurodegeneration Neurodegenerative diseases Neuroscience Neurotoxicity Parkinson's disease Pathogenesis Ribonucleic acid RNA Tumor necrosis factor-TNF Vector-borne diseases |
SummonAdditionalLinks | – databaseName: DOAJ Directory of Open Access Journals dbid: DOA link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV1Nb9NAEF1QT1wQUD4CLRokhISEFWfXznqPBhoVRHNoWtSbtVnvEkv-qOK0ajnxN_h7_BJm1k5oEIIL1-xsvHZeZt54Z98w9hJZbu7GzgXK6CRABi4DhWlYILSRIVeR417x5mg6PjyNPp7FZzdafVFNWCcP3D24IWYoQmn0tDacR1FM4RS_NZkjzdG5UF4JFGPeOpnqfPAYnS7vNiUxBVNDVxc1aXOPSJyS-9Zuv4KQ1-r_E8H8vU7yRuCZ3GN3e8YIabfS--y2rR-w3bTGbLm6hlfgazj9y_HdW_vH0xRmXXU0xiQ4tpdIBFuYVbosQdc5fMbcmE5LAclSrZtdtdA4-NCXZV20kNJ5qxZWDfhQ5h1LU1lvRt19K1-hC1P0M2R-4n-8FibLpoK0um5Wy-Z8URj4pOl8cwkzXDg-iKJ9A2n5dWGLyi5_fPvewvtue8ivjM5f-6NoWyPo2OhNEc4kG_RmVERvczi46it4a1oUiWf31-8nBqnxjdvQ9IhqDr-UhX7ITicHJ-8Og74BRGAiFa4COhkhhXKYdoWJweQmz2MnnMiR1ZiIh7FFX45exY35aGxkZELESJLLWAmbuDgXj9hO3dT2CQNkJU4Ko-aYgEYO7ZBWasytnBy5XMd8wIZrRGSmV0enJh1lhlkSYSjzGMoIQ5nH0IC93sw475RB_mL7lkC2sSNNb_8BIj3rkZ79C-kDtreGaNY7GryG8C3HZIzDLzbD6CJo30fXFlGQcT7yOj9cDtjjDtGblYhQIUWO1IDJLaxvLXV7pC4WXoYcmbREfvz0f9zbM3aHnhYV9_Fkj-2slhd2H9neav7c_7F_Ak-cWGk priority: 102 providerName: Directory of Open Access Journals – databaseName: ProQuest Central dbid: BENPR link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwfV1Lb9NAEF6gvXBBQHkYWjRICAkJq876fUIuJCqIRihpUW-Ws4_Gkh8hThHlxN_g7_FLmFlvAkGo1-ysPLFnv_1mdx6MvUCWK3WktZuKInGRgcduim6Y6xci9ngaaG4q3pyMo-Oz4MN5eG4P3DobVrnGRAPUshV0Rn7YtzjncRi8WXxxqWsU3a7aFhq32C5CcILO1-7RcPxpssbiCMHX3HdGlBuE5Ly_qES3LD3UTdlQve4BFazkpt3bn43J1O__H-n8N3byr81odJfdsSwSsv6z32M3VXOf7WUNetD1FbwEE9dpDsz3bhxMxhlM-4hp3Kdgor4iOexgWhdVBUUj4TP6y5RBBVSqat0Aq4NWw3sbqnXZQUY5WB2sWjDbmwGbtlZGjDr-1iZqF8aIPSR-aj5oB6NlW0NWX7WrZbuYlwI-FpTzXMEUFccXUXavIau-z1VZq-WvHz87eNdfGRnNKCfbpKdtjSDY0ekRziQZRDgKrFcSht9sVG9DSlFBbft8O9HNhGnmhqInFId4UZXFA3Y2Gp6-PXZtUwhXBKm3cilbIvZTja6Ylwg0CilD7WtfItMRAfdChfiOSKMjPohEHAjPmwWJjMPUV4kOpf-Q7TRtox4zQKaiY1-kM3RKA41ySDUL9Ld0PNCyCLnDDtcWkQtbMZ0ad1Q5ek5kQ7mxoZxsKDc25LBXmxmLvlrINbJHZGQbOarzbX5olxe5hY0c_XMfdfI9hf8iCIlM4ppKZkjyC-mngcP21yaaW_DBZ2yWisOeb4YRNuguqGgUWkHO-cDU_uGxwx71Fr3RxPdSpM1B6rB4y9a3VN0eacq5KU2O7DpGzvzkerWestv0HiiUjyf7bGe1vFQHyO1Ws2d2Af8GYfpUog priority: 102 providerName: ProQuest |
Title | RNA Sequencing Reveals Small and Variable Contributions of Infectious Agents to Transcriptomes of Postmortem Nervous Tissues From Amyotrophic Lateral Sclerosis, Alzheimer’s Disease and Parkinson’s Disease Subjects, and Increased Expression of Genes From Disease-Activated Microglia |
URI | https://www.ncbi.nlm.nih.gov/pubmed/30983949 https://www.proquest.com/docview/2306542754 https://www.proquest.com/docview/2210005027 https://pubmed.ncbi.nlm.nih.gov/PMC6447612 https://doaj.org/article/72139a130e0b4459937ca88b020ad394 |
Volume | 13 |
hasFullText | 1 |
inHoldings | 1 |
isFullTextHit | |
isPrint | |
link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwjV3db9MwEDewvfCCgAELjMpICIREWBo7cfKAUAatBqIVale0tyh17DVSPkbSoZW_njsnLSuqEK_xubm457vf2fdByEtAuan2tbZDmQQ2IHBhh-CG2SyRwnFDrl1T8WY09k9n_Mu5d_4nPbpbwGana4f9pGZ1_u76x-oDbPj36HGCvT3WZVZi5e0-lp50mXeH7INdErhNR3xzp-CDIjZ3nz7mCQFQby8td_7ClpEytfx3AdC_4yhvGKbhfXKvQ5Q0akXgAbmtyofkICrBmy5W9BU1MZ7m8PzgljUZR3TaRk-DzaIT9ROAYkOnRZLnNClT-h18Z8ymoli2at0Mq6GVpp-7sK2rhkaYj9XQZUWNqTOKpyqUIcPuv4WJ4KVj0ENIfmb-3IYO66qgUbGqlnV1ucgk_Zpg_nNOp8A4LETWvKVR_muhskLVrxv6qb08MnxhdrZJVLvxHJQeniLBLKQATYcB9iqlg-suurdEhrCwdvfubqIdSdPUDUhHGI94kWfJIzIbDs4-ntpdcwhb8tBZ2pg1IViowSVzAgmOT5p6mmmWAuKR3HU8BXoeNI723b4vBZeOM-dBKryQqUB7KXtM9sqqVIeEAmLRgslwDs4p10AHkDMBv0uLvk4Tz7XI8VoaYtlVTscGHnkMHhTKT2zkJ0b5iY38WOTNZsZlWzXkH7QnKGAbOqz3bR5U9UXcqY8Y_HQGPDFHwVdwD0El7K1gDmA_SVnILXK0Fs94vYdi9C497goPhl9shkF94J1QUiqQgNh1-6YGkCss8qSV5g0nzAkBPvPQImJLzrdY3R4ps4UpUQ4oWwB2fvof731G7uJiYFyfGxyRvWV9pZ4D0FvOe2T_ZDD-NumZg5Ke2c2_AaW1V8Q |
linkProvider | Scholars Portal |
linkToHtml | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwtV3LbtNAFB1KuoANAsrD0MIgARISVpyxHdsLhFyaKKFJhJK06s4445nGkh8hToGw4jf4CT6KL-HesR0IQt11G1_bY-f4zLkz90HIc1C5kWxLqXs8dHVQ4I7ugRummyF3DOZZkqmKN8NRu3divT-zz3bIzzoXBsMqa05URB3lHNfIm2WLc-bY1tvFJx27RuHuat1Co4TFsVh_AZeteNM_gv_3BWPdzvRdT6-6Cujc8oyVjuH2julJ0PKGy-GqUWRLU5oRTJXcYoYtgCAAqrLNWm3uWNwwZpYbObZnClfakQnXvU52LRNcmQbZPeyMPoxr7m8D2av91TbmIoEzUG6MghvoNWUWZ1gfvIUFMplqL_dnIlT9Av4ncv-N1fxr8uveJrcq1Ur9EmZ3yI7I7pI9PwOPPV3Tl1TFkaoF-r1rB-ORTydlhDbMi3QsPoMYLegkDZOEhllET8E_x4wtiqWx6oZbBc0l7VehYRcF9THnq6CrnKrpVJFbngplhh2GUxUlTEfAdWg-VQAqaHeZp9RP1_lqmS_mMaeDEHOsEzqBgcOLiIvX1E--zUWciuWv7z8KelRuUamRYQ64SofbOgLkiqtVcCbaAKNiIL-IaOdrFUWc4aCwgHd1_-pE3eeqeRyYDjHu8TyJw3vk5Ergcp80sjwTDwkFZSQdk3szQI4lwQ6kbQj-nXRaMgptppFmjYiAVxXasVFIEoCnhhgKFIYCxFCgMKSRV5szFmV1kktsDxFkGzusK65-yJfnQUVTgcPAIwhB1wh4CstG8QrfsDsDpyKMTM_SyH4N0aAiO7jH5tPUyLPNYaAp3HsKMwEoCBhrqVpDzNHIgxLRm5GYhgcy3fI04mxhfWuo20eyeK5KoYOad0CjP7p8WE_Jjd50OAgG_dHxY3IT3wmGETJ3nzRWywtxALpyNXtSfcyUfLxq_vgNy4KOwQ |
linkToPdf | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwtV3LbtNAFB1KKiE2CCgPQwuDBEhIWHHGj4kXCLkkUUPbqEpb1J1xxjONJT9CnAJhxW_wK3wOX8K9YzsQhLrrNnMdT5wzZ8713Achz0HlxspTyvRF1DVBgXPTBzfMtCPBLeY7iumKN4cjb-_UeX_mnm2Qn00uDIZVNpyoiTouBL4jb1ctzhl3nbaqwyKOeoO3s08mdpDCk9amnUYFkX25_ALuW_lm2IP_-gVjg_7Juz2z7jBgCse3FiaG3nPbV6Drra6AO8Sxq2xlx7BtCodZrgSyANgqj3U8wR1hWROnG3PXt2VXubEN33udbHLwiqwW2dztj47GzT7gAfHrs1YP85LAMagOScEl9NsqT3KsFd7BYplMt5r7synq3gH_E7z_xm3-tREObpNbtYKlQQW5O2RD5nfJVpCD954t6UuqY0r1y_qtazvjUUCPq2ht2CPpWH4GYVrS4yxKUxrlMf0Avjpmb1Esk9U03yppoeiwDhO7KGmA-V8lXRRUb62a6IpMajPsNpzpiGE6At5D8xMNppIO5kVGg2xZLObFbJoIehBhvnVKj2Hi8CCS8jUN0m9TmWRy_uv7j5L2quMqPTPMB9epcWsjQLT45gquRBtgVwzqlzHtf60jinOcFBbzru9fX2gGQjeSA9NDjIE8T5PoHjm9ErjcJ628yOVDQkElKW4LfwIOsaPADmRuBL6e4h0VRy4zSLtBRCjqau3YNCQNwWtDDIUaQyFiKNQYMsir1RWzqlLJJba7CLKVHdYY1x8U8_OwpqyQM_AOItA4En6F46KQhfXcnYCDEcW27xhku4FoWBMf3GO1TA3ybDUMlIXnUFEuAQUhYx1dd4hxgzyoEL2aiW35INkd3yB8DetrU10fyZOpLosOyp6DXn90-bSekhvAG-HBcLT_mNzER4IRhay7TVqL-YXcAYm5mDyp1zIlH6-aPn4DTSaS9g |
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=RNA+Sequencing+Reveals+Small+and+Variable+Contributions+of+Infectious+Agents+to+Transcriptomes+of+Postmortem+Nervous+Tissues+From+Amyotrophic+Lateral+Sclerosis%2C+Alzheimer%27s+Disease+and+Parkinson%27s+Disease+Subjects%2C+and+Increased+Expression+of+Genes+From+Disease-Activated+Microglia&rft.jtitle=Frontiers+in+neuroscience&rft.au=Bennett%2C+James+P&rft.au=Keeney%2C+Paula+M&rft.au=Brohawn%2C+David+G&rft.date=2019-03-28&rft.issn=1662-4548&rft.volume=13&rft.spage=235&rft_id=info:doi/10.3389%2Ffnins.2019.00235&rft.externalDBID=NO_FULL_TEXT |
thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=1662-453X&client=summon |
thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=1662-453X&client=summon |
thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=1662-453X&client=summon |