The effects of noncoding aquaporin-4 single-nucleotide polymorphisms on cognition and functional progression of Alzheimer's disease

Abstract Introduction The glymphatic system is a brain-wide perivascular network that facilitates clearance of proteins, including amyloid β, from the brain interstitium through the perivascular exchange of cerebrospinal fluid and interstitial fluid. The astrocytic water channel aquaporin-4 (AQP4) i...

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Published inAlzheimer's & dementia : translational research & clinical interventions Vol. 3; no. 3; pp. 348 - 359
Main Authors Burfeind, Kevin G, Murchison, Charles F, Westaway, Shawn K, Simon, Matthew J, Erten-Lyons, Deniz, Kaye, Jeffrey A, Quinn, Joseph F, Iliff, Jeffrey J
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 01.09.2017
John Wiley & Sons, Inc
Elsevier
Subjects
Aging
Alzheimer's disease
Amyloid β
Aquaporin-4
Aquaporins
Cognitive ability
Cognitive decline
Cohort analysis
Cohort study
Datasets
Dementia
Executive function
Genetics
Genomes
Glymphatic system
Localization
Memory
Neurology
Neuropathology
Older people
Other
Pathology
Traumatic brain injury
Oregon
United States > US
Cognitive decline
Glymphatic system
Aquaporin-4
Amyloid β
Cohort study
Genetics
Alzheimer's disease
Online AccessGet full text

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Abstract Abstract Introduction The glymphatic system is a brain-wide perivascular network that facilitates clearance of proteins, including amyloid β, from the brain interstitium through the perivascular exchange of cerebrospinal fluid and interstitial fluid. The astrocytic water channel aquaporin-4 (AQP4) is required for glymphatic system function, and impairment of glymphatic function in the aging brain is associated with altered AQP4 expression and localization. In human cortical tissue, alterations in AQP4 expression and localization are associated with Alzheimer's disease (AD) status and pathology. Although this suggests a potential role for AQP4 in the development or progression of AD, the relationship between of naturally occurring variants in the human AQP4 gene and cognitive function has not yet been evaluated. Methods Using data from several longitudinal aging cohorts, we investigated the association between five AQP4 single-nucleotide polymorphisms (SNPs) and the rate of cognitive decline in participants with a diagnosis of AD. Results None of the five SNPs were associated with different rates of AD diagnosis, age of dementia onset in trial subjects. No association between AQP4 SNPs with histological measures of AD pathology, including Braak stage or neuritic plaque density was observed. However, AQP4 SNPs were associated with altered rates of cognitive decline after AD diagnosis, with two SNPS (rs9951307 and rs3875089) associated with slower cognitive decline and two (rs3763040 and rs3763043) associated with more rapid cognitive decline after AD diagnosis. Discussion These results provide the first evidence that variations in the AQP4 gene, whose gene product AQP4 is vital for glymphatic pathway function, may modulate the progression of cognitive decline in AD.
AbstractList Abstract Introduction The glymphatic system is a brain-wide perivascular network that facilitates clearance of proteins, including amyloid β, from the brain interstitium through the perivascular exchange of cerebrospinal fluid and interstitial fluid. The astrocytic water channel aquaporin-4 (AQP4) is required for glymphatic system function, and impairment of glymphatic function in the aging brain is associated with altered AQP4 expression and localization. In human cortical tissue, alterations in AQP4 expression and localization are associated with Alzheimer's disease (AD) status and pathology. Although this suggests a potential role for AQP4 in the development or progression of AD, the relationship between of naturally occurring variants in the human AQP4 gene and cognitive function has not yet been evaluated. Methods Using data from several longitudinal aging cohorts, we investigated the association between five AQP4 single-nucleotide polymorphisms (SNPs) and the rate of cognitive decline in participants with a diagnosis of AD. Results None of the five SNPs were associated with different rates of AD diagnosis, age of dementia onset in trial subjects. No association between AQP4 SNPs with histological measures of AD pathology, including Braak stage or neuritic plaque density was observed. However, AQP4 SNPs were associated with altered rates of cognitive decline after AD diagnosis, with two SNPS (rs9951307 and rs3875089) associated with slower cognitive decline and two (rs3763040 and rs3763043) associated with more rapid cognitive decline after AD diagnosis. Discussion These results provide the first evidence that variations in the AQP4 gene, whose gene product AQP4 is vital for glymphatic pathway function, may modulate the progression of cognitive decline in AD.
Introduction The glymphatic system is a brain‐wide perivascular network that facilitates clearance of proteins, including amyloid β, from the brain interstitium through the perivascular exchange of cerebrospinal fluid and interstitial fluid. The astrocytic water channel aquaporin‐4 (AQP4) is required for glymphatic system function, and impairment of glymphatic function in the aging brain is associated with altered AQP4 expression and localization. In human cortical tissue, alterations in AQP4 expression and localization are associated with Alzheimer's disease (AD) status and pathology. Although this suggests a potential role for AQP4 in the development or progression of AD, the relationship between of naturally occurring variants in the human AQP4 gene and cognitive function has not yet been evaluated. Methods Using data from several longitudinal aging cohorts, we investigated the association between five AQP4 single‐nucleotide polymorphisms (SNPs) and the rate of cognitive decline in participants with a diagnosis of AD. Results None of the five SNPs were associated with different rates of AD diagnosis, age of dementia onset in trial subjects. No association between AQP4 SNPs with histological measures of AD pathology, including Braak stage or neuritic plaque density was observed. However, AQP4 SNPs were associated with altered rates of cognitive decline after AD diagnosis, with two SNPS (rs9951307 and rs3875089) associated with slower cognitive decline and two (rs3763040 and rs3763043) associated with more rapid cognitive decline after AD diagnosis. Discussion These results provide the first evidence that variations in the AQP4 gene, whose gene product AQP4 is vital for glymphatic pathway function, may modulate the progression of cognitive decline in AD.
The glymphatic system is a brain-wide perivascular network that facilitates clearance of proteins, including amyloid β, from the brain interstitium through the perivascular exchange of cerebrospinal fluid and interstitial fluid. The astrocytic water channel aquaporin-4 (AQP4) is required for glymphatic system function, and impairment of glymphatic function in the aging brain is associated with altered AQP4 expression and localization. In human cortical tissue, alterations in AQP4 expression and localization are associated with Alzheimer's disease (AD) status and pathology. Although this suggests a potential role for AQP4 in the development or progression of AD, the relationship between of naturally occurring variants in the human gene and cognitive function has not yet been evaluated. Using data from several longitudinal aging cohorts, we investigated the association between five single-nucleotide polymorphisms (SNPs) and the rate of cognitive decline in participants with a diagnosis of AD. None of the five SNPs were associated with different rates of AD diagnosis, age of dementia onset in trial subjects. No association between SNPs with histological measures of AD pathology, including Braak stage or neuritic plaque density was observed. However, SNPs were associated with altered rates of cognitive decline after AD diagnosis, with two SNPS (rs9951307 and rs3875089) associated with slower cognitive decline and two (rs3763040 and rs3763043) associated with more rapid cognitive decline after AD diagnosis. These results provide the first evidence that variations in the gene, whose gene product AQP4 is vital for glymphatic pathway function, may modulate the progression of cognitive decline in AD.
The glymphatic system is a brain-wide perivascular network that facilitates clearance of proteins, including amyloid β, from the brain interstitium through the perivascular exchange of cerebrospinal fluid and interstitial fluid. The astrocytic water channel aquaporin-4 (AQP4) is required for glymphatic system function, and impairment of glymphatic function in the aging brain is associated with altered AQP4 expression and localization. In human cortical tissue, alterations in AQP4 expression and localization are associated with Alzheimer's disease (AD) status and pathology. Although this suggests a potential role for AQP4 in the development or progression of AD, the relationship between of naturally occurring variants in the human AQP4 gene and cognitive function has not yet been evaluated. Using data from several longitudinal aging cohorts, we investigated the association between five AQP4 single-nucleotide polymorphisms (SNPs) and the rate of cognitive decline in participants with a diagnosis of AD. None of the five SNPs were associated with different rates of AD diagnosis, age of dementia onset in trial subjects. No association between AQP4 SNPs with histological measures of AD pathology, including Braak stage or neuritic plaque density was observed. However, AQP4 SNPs were associated with altered rates of cognitive decline after AD diagnosis, with two SNPS (rs9951307 and rs3875089) associated with slower cognitive decline and two (rs3763040 and rs3763043) associated with more rapid cognitive decline after AD diagnosis. These results provide the first evidence that variations in the AQP4 gene, whose gene product AQP4 is vital for glymphatic pathway function, may modulate the progression of cognitive decline in AD.
The glymphatic system is a brain-wide perivascular network that facilitates clearance of proteins, including amyloid β, from the brain interstitium through the perivascular exchange of cerebrospinal fluid and interstitial fluid. The astrocytic water channel aquaporin-4 (AQP4) is required for glymphatic system function, and impairment of glymphatic function in the aging brain is associated with altered AQP4 expression and localization. In human cortical tissue, alterations in AQP4 expression and localization are associated with Alzheimer's disease (AD) status and pathology. Although this suggests a potential role for AQP4 in the development or progression of AD, the relationship between of naturally occurring variants in the human AQP4 gene and cognitive function has not yet been evaluated.INTRODUCTIONThe glymphatic system is a brain-wide perivascular network that facilitates clearance of proteins, including amyloid β, from the brain interstitium through the perivascular exchange of cerebrospinal fluid and interstitial fluid. The astrocytic water channel aquaporin-4 (AQP4) is required for glymphatic system function, and impairment of glymphatic function in the aging brain is associated with altered AQP4 expression and localization. In human cortical tissue, alterations in AQP4 expression and localization are associated with Alzheimer's disease (AD) status and pathology. Although this suggests a potential role for AQP4 in the development or progression of AD, the relationship between of naturally occurring variants in the human AQP4 gene and cognitive function has not yet been evaluated.Using data from several longitudinal aging cohorts, we investigated the association between five AQP4 single-nucleotide polymorphisms (SNPs) and the rate of cognitive decline in participants with a diagnosis of AD.METHODSUsing data from several longitudinal aging cohorts, we investigated the association between five AQP4 single-nucleotide polymorphisms (SNPs) and the rate of cognitive decline in participants with a diagnosis of AD.None of the five SNPs were associated with different rates of AD diagnosis, age of dementia onset in trial subjects. No association between AQP4 SNPs with histological measures of AD pathology, including Braak stage or neuritic plaque density was observed. However, AQP4 SNPs were associated with altered rates of cognitive decline after AD diagnosis, with two SNPS (rs9951307 and rs3875089) associated with slower cognitive decline and two (rs3763040 and rs3763043) associated with more rapid cognitive decline after AD diagnosis.RESULTSNone of the five SNPs were associated with different rates of AD diagnosis, age of dementia onset in trial subjects. No association between AQP4 SNPs with histological measures of AD pathology, including Braak stage or neuritic plaque density was observed. However, AQP4 SNPs were associated with altered rates of cognitive decline after AD diagnosis, with two SNPS (rs9951307 and rs3875089) associated with slower cognitive decline and two (rs3763040 and rs3763043) associated with more rapid cognitive decline after AD diagnosis.These results provide the first evidence that variations in the AQP4 gene, whose gene product AQP4 is vital for glymphatic pathway function, may modulate the progression of cognitive decline in AD.DISCUSSIONThese results provide the first evidence that variations in the AQP4 gene, whose gene product AQP4 is vital for glymphatic pathway function, may modulate the progression of cognitive decline in AD.
IntroductionThe glymphatic system is a brain‐wide perivascular network that facilitates clearance of proteins, including amyloid β, from the brain interstitium through the perivascular exchange of cerebrospinal fluid and interstitial fluid. The astrocytic water channel aquaporin‐4 (AQP4) is required for glymphatic system function, and impairment of glymphatic function in the aging brain is associated with altered AQP4 expression and localization. In human cortical tissue, alterations in AQP4 expression and localization are associated with Alzheimer's disease (AD) status and pathology. Although this suggests a potential role for AQP4 in the development or progression of AD, the relationship between of naturally occurring variants in the human AQP4 gene and cognitive function has not yet been evaluated.MethodsUsing data from several longitudinal aging cohorts, we investigated the association between five AQP4 single‐nucleotide polymorphisms (SNPs) and the rate of cognitive decline in participants with a diagnosis of AD.ResultsNone of the five SNPs were associated with different rates of AD diagnosis, age of dementia onset in trial subjects. No association between AQP4 SNPs with histological measures of AD pathology, including Braak stage or neuritic plaque density was observed. However, AQP4 SNPs were associated with altered rates of cognitive decline after AD diagnosis, with two SNPS (rs9951307 and rs3875089) associated with slower cognitive decline and two (rs3763040 and rs3763043) associated with more rapid cognitive decline after AD diagnosis.DiscussionThese results provide the first evidence that variations in the AQP4 gene, whose gene product AQP4 is vital for glymphatic pathway function, may modulate the progression of cognitive decline in AD.
Author Burfeind, Kevin G
Iliff, Jeffrey J
Quinn, Joseph F
Kaye, Jeffrey A
Simon, Matthew J
Erten-Lyons, Deniz
Westaway, Shawn K
Murchison, Charles F
AuthorAffiliation c Knight Cardiovascular Institute, Oregon Health & Science University, Portland, OR, USA
a Department of Anesthesiology and Perioperative Medicine, Oregon Health & Science University, Portland, OR, USA
b Department of Neurology, Oregon Health & Science University, Portland, OR, USA
AuthorAffiliation_xml – name: b Department of Neurology, Oregon Health & Science University, Portland, OR, USA
– name: a Department of Anesthesiology and Perioperative Medicine, Oregon Health & Science University, Portland, OR, USA
– name: c Knight Cardiovascular Institute, Oregon Health & Science University, Portland, OR, USA
Author_xml – sequence: 1
  fullname: Burfeind, Kevin G
– sequence: 2
  fullname: Murchison, Charles F
– sequence: 3
  fullname: Westaway, Shawn K
– sequence: 4
  fullname: Simon, Matthew J
– sequence: 5
  fullname: Erten-Lyons, Deniz
– sequence: 6
  fullname: Kaye, Jeffrey A
– sequence: 7
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– sequence: 8
  fullname: Iliff, Jeffrey J
BackLink https://www.ncbi.nlm.nih.gov/pubmed/29067342$$D View this record in MEDLINE/PubMed
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Cites_doi 10.1002/ana.24271
10.1017/S1355617799544056
10.1038/nrneurol.2015.119
10.1523/JNEUROSCI.3020-14.2014
10.1212/WNL.54.1.105
10.1126/science.1197623
10.1016/S0895-4356(02)00585-1
10.1016/j.jstrokecerebrovasdis.2013.10.017
10.1001/jamaneurol.2015.1285
10.1212/WNL.43.10.1882
10.1016/j.jalz.2011.03.005
10.1093/geronb/gbq095
10.1016/0022-3956(75)90026-6
10.1016/j.jalz.2009.05.663
10.1152/physrev.00011.2013
10.1203/PDR.0b013e3181df4e7c
10.1111/j.1532-5415.1995.tb06377.x
10.1016/j.neurobiolaging.2017.01.017
10.1161/STROKEAHA.107.500785
10.1002/ana.24454
10.1186/alzrt187
10.1126/scitranslmed.3003748
10.1089/neu.2014.3347
10.1001/jamaneurol.2016.4370
10.1001/archneur.65.8.1091
10.1186/s13024-015-0056-1
10.1037/10020-000
10.1172/JCI67677
10.1111/j.1748-0361.2009.00237.x
10.1111/j.1532-5415.1968.tb02103.x
ContentType Journal Article
Copyright The Authors
2017 The Authors
2017 The Authors. Published by Elsevier Inc. on behalf of the Alzheimer's Association.
2017. This work is published under http://creativecommons.org/licenses/by-nc-nd/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
2017 The Authors 2017
Copyright_xml – notice: The Authors
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Issue 3
Keywords Cognitive decline
Glymphatic system
Aquaporin-4
Amyloid β
Cohort study
Genetics
Alzheimer's disease
Language English
License This is an open access article under the CC BY-NC-ND license.
Attribution-NonCommercial-NoDerivs
This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
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content type line 14
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OpenAccessLink https://onlinelibrary.wiley.com/doi/abs/10.1016%2Fj.trci.2017.05.001
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PublicationTitle Alzheimer's & dementia : translational research & clinical interventions
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References Parmelee, Thuras, Katz, Lawton (bib34) 1995; 43
Sutphen, Jasielec, Shah, Macy, Xiong, Vlassenko (bib4) 2015; 72
Brenowitz, Keene, Hawes, Hubbard, Longstreth, Woltjer (bib30) 2017; 53
Iliff, Chen, Plog, Zeppenfeld, Soltero, Yang (bib3) 2014; 34
Kleffner, Bungeroth, Schiffbauer, Schabitz, Ringelstein, Kuhlenbaumer (bib14) 2008; 39
Linn, Linn, Gurel (bib35) 1968; 16
de Groot, Beckerman, Lankhorst, Bouter (bib33) 2003; 56
Wechsler (bib27) 1987
(bib23) 1998; 19
Bates, Mächler, Bolker, Walker (bib32) 2015; 1
Beekly, Ramos, van Belle, Deitrich, Clark, Jacka (bib24) 2004; 18
Dikmen, Heaton, Grant, Temkin (bib29) 1999; 5
Kaye, Maxwell, Mattek, Hayes, Dodge, Pavel (bib18) 2011; 66B
Iliff, Lee, Yu, Feng, Logan, Nedergaard (bib7) 2013; 123
Howieson, Holm, Kaye, Oken, Howieson (bib20) 1993; 43
Tarasoff-Conway, Carare, Osorio, Glodzik, Butler, Fieremans (bib1) 2015; 11
Patterson, Elbert, Mawuenyega, Kasten, Ovod, Ma (bib5) 2015; 78
Green, Kaye, Ball (bib22) 2000; 54
McKhann, Knopman, Chertkow, Hyman, Jack, Kawas (bib21) 2011; 7
Erten-Lyons, Jacobson, Kramer, Grupe, Kaye (bib37) 2010; 6
Eide, Ringstad (bib12) 2015; 4
Mawuenyega, Sigurdson, Ovod, Munsell, Kasten, Morris (bib6) 2010; 330
Dardiotis, Paterakis, Tsivgoulis, Tsintou, Hadjigeorgiou, Dardioti (bib16) 2014; 31
Iliff, Wang, Liao, Plogg, Peng, Gundersen (bib8) 2012; 4
Xu, Xiao, Chen, Huang, Marshall, Gao (bib9) 2015; 10
Nagelhus, Ottersen (bib36) 2013; 93
Yadav, Oh, Kim, Shin (bib15) 2014; 23
Zeppenfeld, Simon, Haswell, D'Abreo, Murchison, Quinn (bib11) 2017; 74
O'Bryant, Waring, Cullum, Hall, Lacritz, Massman (bib26) 2008; 65
Team (bib31) 2016
Zeppenfeld, Simon, Haswell, D'Abreo, Murchison, Quinn (bib38) 2017; 74
Wechsler (bib28) 1939
Folstein, Folstein, McHugh (bib25) 1975; 12
Opdal, Vege, Stray-Pedersen, Rognum (bib13) 2010; 68
Payami, Grimslid, Oken, Camicioli, Sexton, Dame (bib17) 1997; 60
Kaye, Michael, Calvert, Leahy, Crawford, Kramer (bib19) 2009; 25
Wildsmith, Holley, Savage, Skerrett, Landreth (bib2) 2013; 5
Kress, Iliff, Xia, Wang, Wei, Zeppenfeld (bib10) 2014; 76
2015; 78
2015; 1
2009; 25
2015; 4
1997; 60
2015; 72
1993; 43
2015; 11
2015; 10
2008; 39
2013; 123
1975; 12
2013; 93
1939
2013; 5
1999; 5
2014; 23
2011; 7
2003; 56
2017; 53
2017; 74
1998; 19
1968; 16
2010; 68
2004; 18
2011; 66B
2000; 54
1995; 43
2010; 330
1987
2008; 65
2016
2012; 4
2014; 34
2010; 6
2014; 76
2014; 31
e_1_2_7_6_1
e_1_2_7_5_1
e_1_2_7_4_1
Consensus report of the Working Group on: “Molecular and Biochemical Markers of Alzheimer's Disease” (e_1_2_7_24_1) 1998; 19
e_1_2_7_3_1
e_1_2_7_9_1
e_1_2_7_8_1
e_1_2_7_7_1
e_1_2_7_19_1
Team R.C. (e_1_2_7_32_1) 2016
e_1_2_7_17_1
Bates D. (e_1_2_7_33_1) 2015; 1
e_1_2_7_16_1
e_1_2_7_2_1
e_1_2_7_15_1
e_1_2_7_14_1
Beekly D.L. (e_1_2_7_25_1) 2004; 18
e_1_2_7_12_1
e_1_2_7_11_1
e_1_2_7_10_1
Eide P.K. (e_1_2_7_13_1) 2015; 4
e_1_2_7_26_1
e_1_2_7_27_1
e_1_2_7_29_1
e_1_2_7_30_1
e_1_2_7_31_1
e_1_2_7_23_1
e_1_2_7_22_1
e_1_2_7_34_1
e_1_2_7_21_1
e_1_2_7_35_1
e_1_2_7_20_1
e_1_2_7_36_1
Wechsler D. (e_1_2_7_28_1) 1987
e_1_2_7_37_1
e_1_2_7_38_1
e_1_2_7_39_1
Payami H. (e_1_2_7_18_1) 1997; 60
References_xml – volume: 19
  start-page: 109
  year: 1998
  end-page: 116
  ident: bib23
  article-title: The Ronald and Nancy Reagan Research Institute of the Alzheimer's Association and the National Institute on Aging Working Group
  publication-title: Neurobiol Aging
– volume: 54
  start-page: 105
  year: 2000
  end-page: 113
  ident: bib22
  article-title: The Oregon brain aging study: neuropathology accompanying healthy aging in the oldest old
  publication-title: Neurology
– volume: 66B
  start-page: i180
  year: 2011
  end-page: i190
  ident: bib18
  article-title: Intelligent Systems for Assessing Aging Changes: Home-Based, Unobtrusive, and Continuous Assessment of Aging
  publication-title: J Gerontol B Psychol Sci Soc Sci
– volume: 5
  start-page: 33
  year: 2013
  ident: bib2
  article-title: Evidence for impaired amyloid beta clearance in Alzheimer's disease
  publication-title: Alzheimers Res Ther
– volume: 53
  start-page: 83
  year: 2017
  end-page: 92
  ident: bib30
  article-title: Alzheimer's disease neuropathologic change, Lewy body disease, and vascular brain injury in clinic- and community-based samples
  publication-title: Neurobiol Aging
– volume: 31
  start-page: 1920
  year: 2014
  end-page: 1926
  ident: bib16
  article-title: AQP4 tag single nucleotide polymorphisms in patients with traumatic brain injury
  publication-title: J Neurotrauma
– volume: 7
  start-page: 263
  year: 2011
  end-page: 269
  ident: bib21
  article-title: The diagnosis of dementia due to Alzheimer's disease: recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease
  publication-title: Alzheimers Dement
– volume: 1
  start-page: 2015
  year: 2015
  ident: bib32
  article-title: Fitting Linear Mixed-Effects Models Using lme4
  publication-title: J Stat Softw
– volume: 43
  start-page: 1882
  year: 1993
  end-page: 1886
  ident: bib20
  article-title: Neurologic function in the optimally healthy oldest old. Neuropsychological evaluation
  publication-title: Neurology
– volume: 34
  start-page: 16180
  year: 2014
  end-page: 16193
  ident: bib3
  article-title: Impairment of glymphatic pathway function promotes tau pathology after traumatic brain injury
  publication-title: J Neurosci
– volume: 76
  start-page: 845
  year: 2014
  end-page: 861
  ident: bib10
  article-title: Impairment of paravascular clearance pathways in the aging brain
  publication-title: Ann Neurol
– volume: 68
  start-page: 48
  year: 2010
  end-page: 51
  ident: bib13
  article-title: Aquaporin-4 gene variation and sudden infant death syndrome
  publication-title: Pediatr Res
– volume: 74
  start-page: 91
  year: 2017
  end-page: 99
  ident: bib38
  article-title: Preservation of perivascular aquaporin-4 localization in the cognitively-healthy elderly
  publication-title: JAMA Neurol
– volume: 4
  start-page: 147ra11
  year: 2012
  ident: bib8
  article-title: A paravascular pathway facilitates CSF flow through the brain parenchyma and the clearance of interstitial solutes, including amyloid beta
  publication-title: Sci Transl Med
– volume: 72
  start-page: 1029
  year: 2015
  end-page: 1042
  ident: bib4
  article-title: Longitudinal cerebrospinal fluid biomarker changes in preclinical Alzheimer disease during middle age
  publication-title: JAMA Neurol
– volume: 12
  start-page: 189
  year: 1975
  end-page: 198
  ident: bib25
  article-title: “Mini-mental state”: A practical method for grading the cognitive state of patients for the clinician
  publication-title: J Psychiatr Res
– volume: 23
  start-page: 1199
  year: 2014
  end-page: 1206
  ident: bib15
  article-title: Association of rs2075575 and rs9951307 polymorphisms of AQP-4 gene with leukoaraiosis
  publication-title: J Stroke Cerebrovasc Dis
– year: 2016
  ident: bib31
  article-title: R: A Language and Environment for Statistical Computing
– volume: 10
  start-page: 58
  year: 2015
  ident: bib9
  article-title: Deletion of aquaporin-4 in APP/PS1 mice exacerbates brain Abeta accumulation and memory deficits
  publication-title: Mol Neurodegener
– volume: 39
  start-page: 1333
  year: 2008
  end-page: 1335
  ident: bib14
  article-title: The role of aquaporin-4 polymorphisms in the development of brain edema after middle cerebral artery occlusion
  publication-title: Stroke
– volume: 18
  start-page: 270
  year: 2004
  end-page: 277
  ident: bib24
  article-title: The National Alzheimer's Coordinating Center (NACC) Database: an Alzheimer disease database
  publication-title: Alzheimer Dis Assoc Disord
– volume: 56
  start-page: 221
  year: 2003
  end-page: 229
  ident: bib33
  article-title: How to measure comorbidity. a critical review of available methods
  publication-title: J Clin Epidemiol
– volume: 4
  year: 2015
  ident: bib12
  article-title: MRI with intrathecal MRI gadolinium contrast medium administration: a possible method to assess glymphatic function in human brain
  publication-title: Acta Radiol Open
– volume: 78
  start-page: 439
  year: 2015
  end-page: 453
  ident: bib5
  article-title: Age and amyloid effects on human central nervous system amyloid-beta kinetics
  publication-title: Ann Neurol
– volume: 6
  start-page: 118
  year: 2010
  end-page: 124
  ident: bib37
  article-title: The FAS gene, brain volume, and disease progression in Alzheimer's disease
  publication-title: Alzheimers Dement
– volume: 123
  start-page: 1299
  year: 2013
  end-page: 1309
  ident: bib7
  article-title: Brain-wide pathway for waste clearance captured by contrast-enhanced MRI
  publication-title: J Clin Invest
– year: 1987
  ident: bib27
  article-title: Wechsler Memory Scale–Revised
– volume: 16
  start-page: 622
  year: 1968
  end-page: 626
  ident: bib35
  article-title: Cumulative illness rating scale
  publication-title: J Am Geriatr Soc
– volume: 74
  start-page: 91
  year: 2017
  end-page: 99
  ident: bib11
  article-title: Association of perivascular localization of aquaporin-4 with cognition and Alzheimer disease in aging brains
  publication-title: JAMA Neurol
– volume: 25
  start-page: 320
  year: 2009
  end-page: 325
  ident: bib19
  article-title: Exceptional Brain Aging in a Rural Population-Based Cohort
  publication-title: J Rural Health
– volume: 5
  start-page: 346
  year: 1999
  end-page: 356
  ident: bib29
  article-title: Test–retest reliability and practice effects of expanded Halstead–Reitan Neuropsychological Test Battery
  publication-title: J Int Neuropsychol Soc
– volume: 93
  start-page: 1543
  year: 2013
  end-page: 1562
  ident: bib36
  article-title: Physiological roles of aquaporin-4 in brain
  publication-title: Physiol Rev
– year: 1939
  ident: bib28
  article-title: The Measurement and Appraisal of Adult Intelligence
– volume: 60
  start-page: 948
  year: 1997
  end-page: 956
  ident: bib17
  article-title: A prospective study of cognitive health in the elderly (Oregon Brain Aging Study): effects of family history and apolipoprotein E genotype
  publication-title: Am J Hum Genet
– volume: 43
  start-page: 130
  year: 1995
  end-page: 137
  ident: bib34
  article-title: Validation of the Cumulative Illness Rating Scale in a geriatric residential population
  publication-title: J Am Geriatr Soc
– volume: 11
  start-page: 457
  year: 2015
  end-page: 470
  ident: bib1
  article-title: Clearance systems in the brain-implications for Alzheimer disease
  publication-title: Nat Rev Neurol
– volume: 330
  start-page: 1774
  year: 2010
  ident: bib6
  article-title: Decreased clearance of CNS amyloid-β in Alzheimer's disease
  publication-title: Science
– volume: 65
  start-page: 1091
  year: 2008
  end-page: 1095
  ident: bib26
  article-title: Staging dementia using Clinical Dementia Rating Scale Sum of Boxes scores: a Texas Alzheimer's research consortium study
  publication-title: Arch Neurol
– year: 1939
– volume: 123
  start-page: 1299
  year: 2013
  end-page: 1309
  article-title: Brain‐wide pathway for waste clearance captured by contrast‐enhanced MRI
  publication-title: J Clin Invest
– volume: 4
  year: 2015
  article-title: MRI with intrathecal MRI gadolinium contrast medium administration: a possible method to assess glymphatic function in human brain
  publication-title: Acta Radiol Open
– volume: 25
  start-page: 320
  year: 2009
  end-page: 325
  article-title: Exceptional Brain Aging in a Rural Population‐Based Cohort
  publication-title: J Rural Health
– volume: 11
  start-page: 457
  year: 2015
  end-page: 470
  article-title: Clearance systems in the brain‐implications for Alzheimer disease
  publication-title: Nat Rev Neurol
– volume: 34
  start-page: 16180
  year: 2014
  end-page: 16193
  article-title: Impairment of glymphatic pathway function promotes tau pathology after traumatic brain injury
  publication-title: J Neurosci
– volume: 330
  start-page: 1774
  year: 2010
  article-title: Decreased clearance of CNS amyloid‐β in Alzheimer's disease
  publication-title: Science
– volume: 10
  start-page: 58
  year: 2015
  article-title: Deletion of aquaporin‐4 in APP/PS1 mice exacerbates brain Abeta accumulation and memory deficits
  publication-title: Mol Neurodegener
– year: 1987
– volume: 56
  start-page: 221
  year: 2003
  end-page: 229
  article-title: How to measure comorbidity. a critical review of available methods
  publication-title: J Clin Epidemiol
– volume: 93
  start-page: 1543
  year: 2013
  end-page: 1562
  article-title: Physiological roles of aquaporin‐4 in brain
  publication-title: Physiol Rev
– volume: 66B
  start-page: i180
  year: 2011
  end-page: i190
  article-title: Intelligent Systems for Assessing Aging Changes: Home‐Based, Unobtrusive, and Continuous Assessment of Aging
  publication-title: J Gerontol B Psychol Sci Soc Sci
– volume: 6
  start-page: 118
  year: 2010
  end-page: 124
  article-title: The FAS gene, brain volume, and disease progression in Alzheimer's disease
  publication-title: Alzheimers Dement
– volume: 5
  start-page: 33
  year: 2013
  article-title: Evidence for impaired amyloid beta clearance in Alzheimer's disease
  publication-title: Alzheimers Res Ther
– volume: 16
  start-page: 622
  year: 1968
  end-page: 626
  article-title: Cumulative illness rating scale
  publication-title: J Am Geriatr Soc
– volume: 31
  start-page: 1920
  year: 2014
  end-page: 1926
  article-title: AQP4 tag single nucleotide polymorphisms in patients with traumatic brain injury
  publication-title: J Neurotrauma
– year: 2016
– volume: 39
  start-page: 1333
  year: 2008
  end-page: 1335
  article-title: The role of aquaporin‐4 polymorphisms in the development of brain edema after middle cerebral artery occlusion
  publication-title: Stroke
– volume: 23
  start-page: 1199
  year: 2014
  end-page: 1206
  article-title: Association of rs2075575 and rs9951307 polymorphisms of AQP‐4 gene with leukoaraiosis
  publication-title: J Stroke Cerebrovasc Dis
– volume: 43
  start-page: 1882
  year: 1993
  end-page: 1886
  article-title: Neurologic function in the optimally healthy oldest old. Neuropsychological evaluation
  publication-title: Neurology
– volume: 4
  year: 2012
  article-title: A paravascular pathway facilitates CSF flow through the brain parenchyma and the clearance of interstitial solutes, including amyloid beta
  publication-title: Sci Transl Med
– volume: 65
  start-page: 1091
  year: 2008
  end-page: 1095
  article-title: Staging dementia using Clinical Dementia Rating Scale Sum of Boxes scores: a Texas Alzheimer's research consortium study
  publication-title: Arch Neurol
– volume: 18
  start-page: 270
  year: 2004
  end-page: 277
  article-title: The National Alzheimer's Coordinating Center (NACC) Database: an Alzheimer disease database
  publication-title: Alzheimer Dis Assoc Disord
– volume: 5
  start-page: 346
  year: 1999
  end-page: 356
  article-title: Test–retest reliability and practice effects of expanded Halstead–Reitan Neuropsychological Test Battery
  publication-title: J Int Neuropsychol Soc
– volume: 74
  start-page: 91
  year: 2017
  end-page: 99
  article-title: Preservation of perivascular aquaporin‐4 localization in the cognitively‐healthy elderly
  publication-title: JAMA Neurol
– volume: 76
  start-page: 845
  year: 2014
  end-page: 861
  article-title: Impairment of paravascular clearance pathways in the aging brain
  publication-title: Ann Neurol
– volume: 74
  start-page: 91
  year: 2017
  end-page: 99
  article-title: Association of perivascular localization of aquaporin‐4 with cognition and Alzheimer disease in aging brains
  publication-title: JAMA Neurol
– volume: 19
  start-page: 109
  year: 1998
  end-page: 116
  article-title: The Ronald and Nancy Reagan Research Institute of the Alzheimer's Association and the National Institute on Aging Working Group
  publication-title: Neurobiol Aging
– volume: 53
  start-page: 83
  year: 2017
  end-page: 92
  article-title: Alzheimer's disease neuropathologic change, Lewy body disease, and vascular brain injury in clinic‐ and community‐based samples
  publication-title: Neurobiol Aging
– volume: 7
  start-page: 263
  year: 2011
  end-page: 269
  article-title: The diagnosis of dementia due to Alzheimer's disease: recommendations from the National Institute on Aging‐Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease
  publication-title: Alzheimers Dement
– volume: 78
  start-page: 439
  year: 2015
  end-page: 453
  article-title: Age and amyloid effects on human central nervous system amyloid‐beta kinetics
  publication-title: Ann Neurol
– volume: 54
  start-page: 105
  year: 2000
  end-page: 113
  article-title: The Oregon brain aging study: neuropathology accompanying healthy aging in the oldest old
  publication-title: Neurology
– volume: 43
  start-page: 130
  year: 1995
  end-page: 137
  article-title: Validation of the Cumulative Illness Rating Scale in a geriatric residential population
  publication-title: J Am Geriatr Soc
– volume: 68
  start-page: 48
  year: 2010
  end-page: 51
  article-title: Aquaporin‐4 gene variation and sudden infant death syndrome
  publication-title: Pediatr Res
– volume: 1
  start-page: 2015
  year: 2015
  article-title: Fitting Linear Mixed‐Effects Models Using lme4
  publication-title: J Stat Softw
– volume: 60
  start-page: 948
  year: 1997
  end-page: 956
  article-title: A prospective study of cognitive health in the elderly (Oregon Brain Aging Study): effects of family history and apolipoprotein E genotype
  publication-title: Am J Hum Genet
– volume: 12
  start-page: 189
  year: 1975
  end-page: 198
  article-title: “Mini‐mental state”: A practical method for grading the cognitive state of patients for the clinician
  publication-title: J Psychiatr Res
– volume: 72
  start-page: 1029
  year: 2015
  end-page: 1042
  article-title: Longitudinal cerebrospinal fluid biomarker changes in preclinical Alzheimer disease during middle age
  publication-title: JAMA Neurol
– ident: e_1_2_7_11_1
  doi: 10.1002/ana.24271
– volume: 60
  start-page: 948
  year: 1997
  ident: e_1_2_7_18_1
  article-title: A prospective study of cognitive health in the elderly (Oregon Brain Aging Study): effects of family history and apolipoprotein E genotype
  publication-title: Am J Hum Genet
– volume: 19
  start-page: 109
  year: 1998
  ident: e_1_2_7_24_1
  article-title: The Ronald and Nancy Reagan Research Institute of the Alzheimer's Association and the National Institute on Aging Working Group
  publication-title: Neurobiol Aging
– ident: e_1_2_7_30_1
  doi: 10.1017/S1355617799544056
– ident: e_1_2_7_2_1
  doi: 10.1038/nrneurol.2015.119
– ident: e_1_2_7_4_1
  doi: 10.1523/JNEUROSCI.3020-14.2014
– ident: e_1_2_7_23_1
  doi: 10.1212/WNL.54.1.105
– ident: e_1_2_7_7_1
  doi: 10.1126/science.1197623
– ident: e_1_2_7_34_1
  doi: 10.1016/S0895-4356(02)00585-1
– ident: e_1_2_7_16_1
  doi: 10.1016/j.jstrokecerebrovasdis.2013.10.017
– ident: e_1_2_7_5_1
  doi: 10.1001/jamaneurol.2015.1285
– ident: e_1_2_7_21_1
  doi: 10.1212/WNL.43.10.1882
– ident: e_1_2_7_22_1
  doi: 10.1016/j.jalz.2011.03.005
– ident: e_1_2_7_19_1
  doi: 10.1093/geronb/gbq095
– ident: e_1_2_7_26_1
  doi: 10.1016/0022-3956(75)90026-6
– ident: e_1_2_7_38_1
  doi: 10.1016/j.jalz.2009.05.663
– ident: e_1_2_7_37_1
  doi: 10.1152/physrev.00011.2013
– ident: e_1_2_7_14_1
  doi: 10.1203/PDR.0b013e3181df4e7c
– ident: e_1_2_7_35_1
  doi: 10.1111/j.1532-5415.1995.tb06377.x
– ident: e_1_2_7_31_1
  doi: 10.1016/j.neurobiolaging.2017.01.017
– ident: e_1_2_7_15_1
  doi: 10.1161/STROKEAHA.107.500785
– volume: 18
  start-page: 270
  year: 2004
  ident: e_1_2_7_25_1
  article-title: The National Alzheimer's Coordinating Center (NACC) Database: an Alzheimer disease database
  publication-title: Alzheimer Dis Assoc Disord
– volume-title: Wechsler Memory Scale–Revised
  year: 1987
  ident: e_1_2_7_28_1
– ident: e_1_2_7_6_1
  doi: 10.1002/ana.24454
– ident: e_1_2_7_3_1
  doi: 10.1186/alzrt187
– ident: e_1_2_7_9_1
  doi: 10.1126/scitranslmed.3003748
– ident: e_1_2_7_17_1
  doi: 10.1089/neu.2014.3347
– volume: 4
  year: 2015
  ident: e_1_2_7_13_1
  article-title: MRI with intrathecal MRI gadolinium contrast medium administration: a possible method to assess glymphatic function in human brain
  publication-title: Acta Radiol Open
– ident: e_1_2_7_39_1
  doi: 10.1001/jamaneurol.2016.4370
– volume-title: R: A Language and Environment for Statistical Computing
  year: 2016
  ident: e_1_2_7_32_1
– ident: e_1_2_7_27_1
  doi: 10.1001/archneur.65.8.1091
– ident: e_1_2_7_10_1
  doi: 10.1186/s13024-015-0056-1
– ident: e_1_2_7_12_1
  doi: 10.1001/jamaneurol.2016.4370
– ident: e_1_2_7_29_1
  doi: 10.1037/10020-000
– ident: e_1_2_7_8_1
  doi: 10.1172/JCI67677
– volume: 1
  start-page: 2015
  year: 2015
  ident: e_1_2_7_33_1
  article-title: Fitting Linear Mixed‐Effects Models Using lme4
  publication-title: J Stat Softw
– ident: e_1_2_7_20_1
  doi: 10.1111/j.1748-0361.2009.00237.x
– ident: e_1_2_7_36_1
  doi: 10.1111/j.1532-5415.1968.tb02103.x
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Snippet Abstract Introduction The glymphatic system is a brain-wide perivascular network that facilitates clearance of proteins, including amyloid β, from the brain...
The glymphatic system is a brain-wide perivascular network that facilitates clearance of proteins, including amyloid β, from the brain interstitium through the...
Introduction The glymphatic system is a brain‐wide perivascular network that facilitates clearance of proteins, including amyloid β, from the brain...
IntroductionThe glymphatic system is a brain‐wide perivascular network that facilitates clearance of proteins, including amyloid β, from the brain interstitium...
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StartPage 348
SubjectTerms Aging
Alzheimer's disease
Amyloid β
Aquaporin-4
Aquaporins
Cognitive ability
Cognitive decline
Cohort analysis
Cohort study
Datasets
Dementia
Executive function
Genetics
Genomes
Glymphatic system
Localization
Memory
Neurology
Neuropathology
Older people
Other
Pathology
Traumatic brain injury
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Title The effects of noncoding aquaporin-4 single-nucleotide polymorphisms on cognition and functional progression of Alzheimer's disease
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https://dx.doi.org/10.1016/j.trci.2017.05.001
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