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Multiscale Analysis of Independent Alzheimer’s Cohorts Finds Disruption of Molecular, Genetic, and Clinical Networks by Human Herpesvirus

Investigators have long suspected that pathogenic microbes might contribute to the onset and progression of Alzheimer’s disease (AD) although definitive evidence has not been presented. Whether such findings represent a causal contribution, or reflect opportunistic passengers of neurodegeneration, i... Full description

Journal Title: Neuron (Cambridge Mass.), 2018-07-11, Vol.99 (1), p.64-82.e7
Main Author: Readhead, Ben
Other Authors: Haure-Mirande, Jean-Vianney , Funk, Cory C , Richards, Matthew A , Shannon, Paul , Haroutunian, Vahram , Sano, Mary , Liang, Winnie S , Beckmann, Noam D , Price, Nathan D , Reiman, Eric M , Schadt, Eric E , Ehrlich, Michelle E , Gandy, Sam , Dudley, Joel T
Format: Electronic Article Electronic Article
Language: English
Subjects:
Quelle: Alma/SFX Local Collection
Publisher: United States: Elsevier Inc
ID: ISSN: 0896-6273
Link: https://www.ncbi.nlm.nih.gov/pubmed/29937276
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title: Multiscale Analysis of Independent Alzheimer’s Cohorts Finds Disruption of Molecular, Genetic, and Clinical Networks by Human Herpesvirus
format: Article
creator:
  • Readhead, Ben
  • Haure-Mirande, Jean-Vianney
  • Funk, Cory C
  • Richards, Matthew A
  • Shannon, Paul
  • Haroutunian, Vahram
  • Sano, Mary
  • Liang, Winnie S
  • Beckmann, Noam D
  • Price, Nathan D
  • Reiman, Eric M
  • Schadt, Eric E
  • Ehrlich, Michelle E
  • Gandy, Sam
  • Dudley, Joel T
subjects:
  • Adaptor Proteins, Signal Transducing - genetics
  • Alzheimer Disease - genetics
  • Alzheimer Disease - metabolism
  • Alzheimer Disease - pathology
  • Alzheimer Disease - virology
  • Alzheimer's disease
  • Amyloid beta-Protein Precursor - metabolism
  • Amyloid Precursor Protein Secretases - genetics
  • Animals
  • Aspartic Acid Endopeptidases - genetics
  • b-Site APP cleaving enzyme 1
  • Brain
  • Brain - metabolism
  • Brain - pathology
  • Brain - virology
  • Brain research
  • Case-Control Studies
  • Clusterin - genetics
  • Cohort Studies
  • Data collection
  • Development and progression
  • Encephalitis, Viral - genetics
  • Encephalitis, Viral - metabolism
  • Encephalitis, Viral - pathology
  • Encephalitis, Viral - virology
  • Gene expression
  • Gene Expression Profiling
  • Gene Regulatory Networks
  • Genetic research
  • Genomics
  • Herpes simplex
  • Herpesviridae
  • Herpesvirus 6, Human
  • Herpesvirus 7, Human
  • HHV-6A
  • HHV-6B
  • HHV-7
  • human herpesvirus
  • Humans
  • integrative genomics
  • Medical colleges
  • Medical research
  • Medicine, Experimental
  • Mice
  • Mice, Knockout
  • Mice, Transgenic
  • Microbiota
  • MicroRNAs - genetics
  • Monomeric Clathrin Assembly Proteins - genetics
  • multiscale networks
  • network biology
  • Neurodegeneration
  • Neuromodulation
  • Neuropathology
  • Nuclear Proteins - genetics
  • Presenilin-1 - genetics
  • Protein turnover
  • Proteins
  • Proteomics
  • Roseolovirus
  • Roseolovirus Infections - genetics
  • Roseolovirus Infections - metabolism
  • Roseolovirus Infections - pathology
  • Roseolovirus Infections - virology
  • systems biology
  • Tumor Suppressor Proteins - genetics
  • Viral Load
  • Viruses
ispartof: Neuron (Cambridge, Mass.), 2018-07-11, Vol.99 (1), p.64-82.e7
description: Investigators have long suspected that pathogenic microbes might contribute to the onset and progression of Alzheimer’s disease (AD) although definitive evidence has not been presented. Whether such findings represent a causal contribution, or reflect opportunistic passengers of neurodegeneration, is also difficult to resolve. We constructed multiscale networks of the late-onset AD-associated virome, integrating genomic, transcriptomic, proteomic, and histopathological data across four brain regions from human post-mortem tissue. We observed increased human herpesvirus 6A (HHV-6A) and human herpesvirus 7 (HHV-7) from subjects with AD compared with controls. These results were replicated in two additional, independent and geographically dispersed cohorts. We observed regulatory relationships linking viral abundance and modulators of APP metabolism, including induction of APBB2, APPBP2, BIN1, BACE1, CLU, PICALM, and PSEN1 by HHV-6A. This study elucidates networks linking molecular, clinical, and neuropathological features with viral activity and is consistent with viral activity constituting a general feature of AD. •Common viral species frequently detected in normal, aging brain•Increased HHV-6A and HHV-7 in brains of subjects with Alzheimer’s disease (AD)•Findings were replicated in two additional, independent cohorts•Multiscale networks reveal viral regulation of AD risk, and APP processing genes Readhead et al. construct multiscale networks of the late-onset Alzheimer’s disease (AD)-associated virome and observe pathogenic regulation of molecular, clinical, and neuropathological networks by several common viruses, particularly human herpesvirus 6A and human herpesvirus 7.
language: eng
source: Alma/SFX Local Collection
identifier: ISSN: 0896-6273
fulltext: fulltext
issn:
  • 0896-6273
  • 1097-4199
url: Link


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titleMultiscale Analysis of Independent Alzheimer’s Cohorts Finds Disruption of Molecular, Genetic, and Clinical Networks by Human Herpesvirus
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creatorReadhead, Ben ; Haure-Mirande, Jean-Vianney ; Funk, Cory C ; Richards, Matthew A ; Shannon, Paul ; Haroutunian, Vahram ; Sano, Mary ; Liang, Winnie S ; Beckmann, Noam D ; Price, Nathan D ; Reiman, Eric M ; Schadt, Eric E ; Ehrlich, Michelle E ; Gandy, Sam ; Dudley, Joel T
creatorcontribReadhead, Ben ; Haure-Mirande, Jean-Vianney ; Funk, Cory C ; Richards, Matthew A ; Shannon, Paul ; Haroutunian, Vahram ; Sano, Mary ; Liang, Winnie S ; Beckmann, Noam D ; Price, Nathan D ; Reiman, Eric M ; Schadt, Eric E ; Ehrlich, Michelle E ; Gandy, Sam ; Dudley, Joel T
descriptionInvestigators have long suspected that pathogenic microbes might contribute to the onset and progression of Alzheimer’s disease (AD) although definitive evidence has not been presented. Whether such findings represent a causal contribution, or reflect opportunistic passengers of neurodegeneration, is also difficult to resolve. We constructed multiscale networks of the late-onset AD-associated virome, integrating genomic, transcriptomic, proteomic, and histopathological data across four brain regions from human post-mortem tissue. We observed increased human herpesvirus 6A (HHV-6A) and human herpesvirus 7 (HHV-7) from subjects with AD compared with controls. These results were replicated in two additional, independent and geographically dispersed cohorts. We observed regulatory relationships linking viral abundance and modulators of APP metabolism, including induction of APBB2, APPBP2, BIN1, BACE1, CLU, PICALM, and PSEN1 by HHV-6A. This study elucidates networks linking molecular, clinical, and neuropathological features with viral activity and is consistent with viral activity constituting a general feature of AD. •Common viral species frequently detected in normal, aging brain•Increased HHV-6A and HHV-7 in brains of subjects with Alzheimer’s disease (AD)•Findings were replicated in two additional, independent cohorts•Multiscale networks reveal viral regulation of AD risk, and APP processing genes Readhead et al. construct multiscale networks of the late-onset Alzheimer’s disease (AD)-associated virome and observe pathogenic regulation of molecular, clinical, and neuropathological networks by several common viruses, particularly human herpesvirus 6A and human herpesvirus 7.
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0ISSN: 0896-6273
1EISSN: 1097-4199
2DOI: 10.1016/j.neuron.2018.05.023
3PMID: 29937276
languageeng
publisherUnited States: Elsevier Inc
subjectAdaptor Proteins, Signal Transducing - genetics ; Alzheimer Disease - genetics ; Alzheimer Disease - metabolism ; Alzheimer Disease - pathology ; Alzheimer Disease - virology ; Alzheimer's disease ; Amyloid beta-Protein Precursor - metabolism ; Amyloid Precursor Protein Secretases - genetics ; Animals ; Aspartic Acid Endopeptidases - genetics ; b-Site APP cleaving enzyme 1 ; Brain ; Brain - metabolism ; Brain - pathology ; Brain - virology ; Brain research ; Case-Control Studies ; Clusterin - genetics ; Cohort Studies ; Data collection ; Development and progression ; Encephalitis, Viral - genetics ; Encephalitis, Viral - metabolism ; Encephalitis, Viral - pathology ; Encephalitis, Viral - virology ; Gene expression ; Gene Expression Profiling ; Gene Regulatory Networks ; Genetic research ; Genomics ; Herpes simplex ; Herpesviridae ; Herpesvirus 6, Human ; Herpesvirus 7, Human ; HHV-6A ; HHV-6B ; HHV-7 ; human herpesvirus ; Humans ; integrative genomics ; Medical colleges ; Medical research ; Medicine, Experimental ; Mice ; Mice, Knockout ; Mice, Transgenic ; Microbiota ; MicroRNAs - genetics ; Monomeric Clathrin Assembly Proteins - genetics ; multiscale networks ; network biology ; Neurodegeneration ; Neuromodulation ; Neuropathology ; Nuclear Proteins - genetics ; Presenilin-1 - genetics ; Protein turnover ; Proteins ; Proteomics ; Roseolovirus ; Roseolovirus Infections - genetics ; Roseolovirus Infections - metabolism ; Roseolovirus Infections - pathology ; Roseolovirus Infections - virology ; systems biology ; Tumor Suppressor Proteins - genetics ; Viral Load ; Viruses
ispartofNeuron (Cambridge, Mass.), 2018-07-11, Vol.99 (1), p.64-82.e7
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02018 Elsevier Inc.
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0Readhead, Ben
1Haure-Mirande, Jean-Vianney
2Funk, Cory C
3Richards, Matthew A
4Shannon, Paul
5Haroutunian, Vahram
6Sano, Mary
7Liang, Winnie S
8Beckmann, Noam D
9Price, Nathan D
10Reiman, Eric M
11Schadt, Eric E
12Ehrlich, Michelle E
13Gandy, Sam
14Dudley, Joel T
title
0Multiscale Analysis of Independent Alzheimer’s Cohorts Finds Disruption of Molecular, Genetic, and Clinical Networks by Human Herpesvirus
1Neuron (Cambridge, Mass.)
addtitleNeuron
descriptionInvestigators have long suspected that pathogenic microbes might contribute to the onset and progression of Alzheimer’s disease (AD) although definitive evidence has not been presented. Whether such findings represent a causal contribution, or reflect opportunistic passengers of neurodegeneration, is also difficult to resolve. We constructed multiscale networks of the late-onset AD-associated virome, integrating genomic, transcriptomic, proteomic, and histopathological data across four brain regions from human post-mortem tissue. We observed increased human herpesvirus 6A (HHV-6A) and human herpesvirus 7 (HHV-7) from subjects with AD compared with controls. These results were replicated in two additional, independent and geographically dispersed cohorts. We observed regulatory relationships linking viral abundance and modulators of APP metabolism, including induction of APBB2, APPBP2, BIN1, BACE1, CLU, PICALM, and PSEN1 by HHV-6A. This study elucidates networks linking molecular, clinical, and neuropathological features with viral activity and is consistent with viral activity constituting a general feature of AD. •Common viral species frequently detected in normal, aging brain•Increased HHV-6A and HHV-7 in brains of subjects with Alzheimer’s disease (AD)•Findings were replicated in two additional, independent cohorts•Multiscale networks reveal viral regulation of AD risk, and APP processing genes Readhead et al. construct multiscale networks of the late-onset Alzheimer’s disease (AD)-associated virome and observe pathogenic regulation of molecular, clinical, and neuropathological networks by several common viruses, particularly human herpesvirus 6A and human herpesvirus 7.
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0Adaptor Proteins, Signal Transducing - genetics
1Alzheimer Disease - genetics
2Alzheimer Disease - metabolism
3Alzheimer Disease - pathology
4Alzheimer Disease - virology
5Alzheimer's disease
6Amyloid beta-Protein Precursor - metabolism
7Amyloid Precursor Protein Secretases - genetics
8Animals
9Aspartic Acid Endopeptidases - genetics
10b-Site APP cleaving enzyme 1
11Brain
12Brain - metabolism
13Brain - pathology
14Brain - virology
15Brain research
16Case-Control Studies
17Clusterin - genetics
18Cohort Studies
19Data collection
20Development and progression
21Encephalitis, Viral - genetics
22Encephalitis, Viral - metabolism
23Encephalitis, Viral - pathology
24Encephalitis, Viral - virology
25Gene expression
26Gene Expression Profiling
27Gene Regulatory Networks
28Genetic research
29Genomics
30Herpes simplex
31Herpesviridae
32Herpesvirus 6, Human
33Herpesvirus 7, Human
34HHV-6A
35HHV-6B
36HHV-7
37human herpesvirus
38Humans
39integrative genomics
40Medical colleges
41Medical research
42Medicine, Experimental
43Mice
44Mice, Knockout
45Mice, Transgenic
46Microbiota
47MicroRNAs - genetics
48Monomeric Clathrin Assembly Proteins - genetics
49multiscale networks
50network biology
51Neurodegeneration
52Neuromodulation
53Neuropathology
54Nuclear Proteins - genetics
55Presenilin-1 - genetics
56Protein turnover
57Proteins
58Proteomics
59Roseolovirus
60Roseolovirus Infections - genetics
61Roseolovirus Infections - metabolism
62Roseolovirus Infections - pathology
63Roseolovirus Infections - virology
64systems biology
65Tumor Suppressor Proteins - genetics
66Viral Load
67Viruses
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8Beckmann, Noam D
9Price, Nathan D
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titleMultiscale Analysis of Independent Alzheimer’s Cohorts Finds Disruption of Molecular, Genetic, and Clinical Networks by Human Herpesvirus
authorReadhead, Ben ; Haure-Mirande, Jean-Vianney ; Funk, Cory C ; Richards, Matthew A ; Shannon, Paul ; Haroutunian, Vahram ; Sano, Mary ; Liang, Winnie S ; Beckmann, Noam D ; Price, Nathan D ; Reiman, Eric M ; Schadt, Eric E ; Ehrlich, Michelle E ; Gandy, Sam ; Dudley, Joel T
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1Alzheimer Disease - genetics
2Alzheimer Disease - metabolism
3Alzheimer Disease - pathology
4Alzheimer Disease - virology
5Alzheimer's disease
6Amyloid beta-Protein Precursor - metabolism
7Amyloid Precursor Protein Secretases - genetics
8Animals
9Aspartic Acid Endopeptidases - genetics
10b-Site APP cleaving enzyme 1
11Brain
12Brain - metabolism
13Brain - pathology
14Brain - virology
15Brain research
16Case-Control Studies
17Clusterin - genetics
18Cohort Studies
19Data collection
20Development and progression
21Encephalitis, Viral - genetics
22Encephalitis, Viral - metabolism
23Encephalitis, Viral - pathology
24Encephalitis, Viral - virology
25Gene expression
26Gene Expression Profiling
27Gene Regulatory Networks
28Genetic research
29Genomics
30Herpes simplex
31Herpesviridae
32Herpesvirus 6, Human
33Herpesvirus 7, Human
34HHV-6A
35HHV-6B
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37human herpesvirus
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45Mice, Transgenic
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52Neuromodulation
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57Proteins
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60Roseolovirus Infections - genetics
61Roseolovirus Infections - metabolism
62Roseolovirus Infections - pathology
63Roseolovirus Infections - virology
64systems biology
65Tumor Suppressor Proteins - genetics
66Viral Load
67Viruses
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abstractInvestigators have long suspected that pathogenic microbes might contribute to the onset and progression of Alzheimer’s disease (AD) although definitive evidence has not been presented. Whether such findings represent a causal contribution, or reflect opportunistic passengers of neurodegeneration, is also difficult to resolve. We constructed multiscale networks of the late-onset AD-associated virome, integrating genomic, transcriptomic, proteomic, and histopathological data across four brain regions from human post-mortem tissue. We observed increased human herpesvirus 6A (HHV-6A) and human herpesvirus 7 (HHV-7) from subjects with AD compared with controls. These results were replicated in two additional, independent and geographically dispersed cohorts. We observed regulatory relationships linking viral abundance and modulators of APP metabolism, including induction of APBB2, APPBP2, BIN1, BACE1, CLU, PICALM, and PSEN1 by HHV-6A. This study elucidates networks linking molecular, clinical, and neuropathological features with viral activity and is consistent with viral activity constituting a general feature of AD. •Common viral species frequently detected in normal, aging brain•Increased HHV-6A and HHV-7 in brains of subjects with Alzheimer’s disease (AD)•Findings were replicated in two additional, independent cohorts•Multiscale networks reveal viral regulation of AD risk, and APP processing genes Readhead et al. construct multiscale networks of the late-onset Alzheimer’s disease (AD)-associated virome and observe pathogenic regulation of molecular, clinical, and neuropathological networks by several common viruses, particularly human herpesvirus 6A and human herpesvirus 7.
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