Increased Cortical Thickness in Alzheimer's Disease

Patients with Alzheimer's disease (AD) have diffuse brain atrophy, but some regions, such as the anterior cingulate cortex (ACC), are spared and may even show increase in size compared to controls. The extent, clinical significance, and mechanisms associated with increased cortical thickness in...

Full description

Saved in:
Bibliographic Details
Published inAnnals of neurology Vol. 95; no. 5; pp. 929 - 940
Main Authors Phan, Tony X., Baratono, Sheena, Drew, William, Tetreault, Aaron M., Fox, Michael D., Darby, R. Ryan
Format Journal Article
LanguageEnglish
Published United States Wiley Subscription Services, Inc 01.05.2024
Subjects
Aged
Aged, 80 and over
Alzheimer Disease - diagnostic imaging
Alzheimer Disease - pathology
Alzheimer's disease
Atrophy
Atrophy - pathology
Brain
Brain Cortical Thickness
Brain mapping
Cerebral Cortex - diagnostic imaging
Cerebral Cortex - pathology
Cognitive ability
Cortex (cingulate)
Cross-Sectional Studies
Dementia disorders
Female
Frontotemporal dementia
Gyrus Cinguli - diagnostic imaging
Gyrus Cinguli - pathology
Humans
Magnetic Resonance Imaging
Male
Medical imaging
Middle Aged
Neurodegenerative diseases
Neuroimaging
Neuroplasticity
Signs and symptoms
Thickness
Visual cortex
Online AccessGet full text

Cover

Abstract Patients with Alzheimer's disease (AD) have diffuse brain atrophy, but some regions, such as the anterior cingulate cortex (ACC), are spared and may even show increase in size compared to controls. The extent, clinical significance, and mechanisms associated with increased cortical thickness in AD remain unknown. Recent work suggested neural facilitation of regions anticorrelated to atrophied regions in frontotemporal dementia. Here, we aim to determine whether increased thickness occurs in sporadic AD, whether it relates to clinical symptoms, and whether it occur in brain regions functionally connected to-but anticorrelated with-locations of atrophy. Cross-sectional clinical, neuropsychological, and neuroimaging data from the Alzheimer's Disease Neuroimaging Initiative were analyzed to investigate cortical thickness in AD subjects versus controls. Atrophy network mapping was used to identify brain regions functionally connected to locations of increased thickness and atrophy. AD patients showed increased thickness in the ACC in a region-of-interest analysis and the visual cortex in an exploratory analysis. Increased thickness in the left ACC was associated with preserved cognitive function, while increased thickness in the left visual cortex was associated with hallucinations. Finally, we found that locations of increased thickness were functionally connected to, but anticorrelated with, locations of brain atrophy (r = -0.81, p < 0.05). Our results suggest that increased cortical thickness in Alzheimer's disease is relevant to AD symptoms and preferentially occur in brain regions functionally connected to, but anticorrelated with, areas of brain atrophy. Implications for models of compensatory neuroplasticity in response to neurodegeneration are discussed. ANN NEUROL 2024;95:929-940.
AbstractList Patients with Alzheimer's disease (AD) have diffuse brain atrophy, but some regions, such as the anterior cingulate cortex (ACC), are spared and may even show increase in size compared to controls. The extent, clinical significance, and mechanisms associated with increased cortical thickness in AD remain unknown. Recent work suggested neural facilitation of regions anticorrelated to atrophied regions in frontotemporal dementia. Here, we aim to determine whether increased thickness occurs in sporadic AD, whether it relates to clinical symptoms, and whether it occur in brain regions functionally connected to-but anticorrelated with-locations of atrophy.OBJECTIVEPatients with Alzheimer's disease (AD) have diffuse brain atrophy, but some regions, such as the anterior cingulate cortex (ACC), are spared and may even show increase in size compared to controls. The extent, clinical significance, and mechanisms associated with increased cortical thickness in AD remain unknown. Recent work suggested neural facilitation of regions anticorrelated to atrophied regions in frontotemporal dementia. Here, we aim to determine whether increased thickness occurs in sporadic AD, whether it relates to clinical symptoms, and whether it occur in brain regions functionally connected to-but anticorrelated with-locations of atrophy.Cross-sectional clinical, neuropsychological, and neuroimaging data from the Alzheimer's Disease Neuroimaging Initiative were analyzed to investigate cortical thickness in AD subjects versus controls. Atrophy network mapping was used to identify brain regions functionally connected to locations of increased thickness and atrophy.METHODSCross-sectional clinical, neuropsychological, and neuroimaging data from the Alzheimer's Disease Neuroimaging Initiative were analyzed to investigate cortical thickness in AD subjects versus controls. Atrophy network mapping was used to identify brain regions functionally connected to locations of increased thickness and atrophy.AD patients showed increased thickness in the ACC in a region-of-interest analysis and the visual cortex in an exploratory analysis. Increased thickness in the left ACC was associated with preserved cognitive function, while increased thickness in the left visual cortex was associated with hallucinations. Finally, we found that locations of increased thickness were functionally connected to, but anticorrelated with, locations of brain atrophy (r = -0.81, p < 0.05).RESULTSAD patients showed increased thickness in the ACC in a region-of-interest analysis and the visual cortex in an exploratory analysis. Increased thickness in the left ACC was associated with preserved cognitive function, while increased thickness in the left visual cortex was associated with hallucinations. Finally, we found that locations of increased thickness were functionally connected to, but anticorrelated with, locations of brain atrophy (r = -0.81, p < 0.05).Our results suggest that increased cortical thickness in Alzheimer's disease is relevant to AD symptoms and preferentially occur in brain regions functionally connected to, but anticorrelated with, areas of brain atrophy. Implications for models of compensatory neuroplasticity in response to neurodegeneration are discussed. ANN NEUROL 2024;95:929-940.INTERPRETATIONOur results suggest that increased cortical thickness in Alzheimer's disease is relevant to AD symptoms and preferentially occur in brain regions functionally connected to, but anticorrelated with, areas of brain atrophy. Implications for models of compensatory neuroplasticity in response to neurodegeneration are discussed. ANN NEUROL 2024;95:929-940.
Patients with Alzheimer's disease (AD) have diffuse brain atrophy, but some regions, such as the anterior cingulate cortex (ACC), are spared and may even show increase in size compared to controls. The extent, clinical significance, and mechanisms associated with increased cortical thickness in AD remain unknown. Recent work suggested neural facilitation of regions anticorrelated to atrophied regions in frontotemporal dementia. Here, we aim to determine whether increased thickness occurs in sporadic AD, whether it relates to clinical symptoms, and whether it occur in brain regions functionally connected to-but anticorrelated with-locations of atrophy. Cross-sectional clinical, neuropsychological, and neuroimaging data from the Alzheimer's Disease Neuroimaging Initiative were analyzed to investigate cortical thickness in AD subjects versus controls. Atrophy network mapping was used to identify brain regions functionally connected to locations of increased thickness and atrophy. AD patients showed increased thickness in the ACC in a region-of-interest analysis and the visual cortex in an exploratory analysis. Increased thickness in the left ACC was associated with preserved cognitive function, while increased thickness in the left visual cortex was associated with hallucinations. Finally, we found that locations of increased thickness were functionally connected to, but anticorrelated with, locations of brain atrophy (r = -0.81, p < 0.05). Our results suggest that increased cortical thickness in Alzheimer's disease is relevant to AD symptoms and preferentially occur in brain regions functionally connected to, but anticorrelated with, areas of brain atrophy. Implications for models of compensatory neuroplasticity in response to neurodegeneration are discussed. ANN NEUROL 2024;95:929-940.
ObjectivePatients with Alzheimer's disease (AD) have diffuse brain atrophy, but some regions, such as the anterior cingulate cortex (ACC), are spared and may even show increase in size compared to controls. The extent, clinical significance, and mechanisms associated with increased cortical thickness in AD remain unknown. Recent work suggested neural facilitation of regions anticorrelated to atrophied regions in frontotemporal dementia. Here, we aim to determine whether increased thickness occurs in sporadic AD, whether it relates to clinical symptoms, and whether it occur in brain regions functionally connected to—but anticorrelated with—locations of atrophy.MethodsCross‐sectional clinical, neuropsychological, and neuroimaging data from the Alzheimer's Disease Neuroimaging Initiative were analyzed to investigate cortical thickness in AD subjects versus controls. Atrophy network mapping was used to identify brain regions functionally connected to locations of increased thickness and atrophy.ResultsAD patients showed increased thickness in the ACC in a region‐of‐interest analysis and the visual cortex in an exploratory analysis. Increased thickness in the left ACC was associated with preserved cognitive function, while increased thickness in the left visual cortex was associated with hallucinations. Finally, we found that locations of increased thickness were functionally connected to, but anticorrelated with, locations of brain atrophy (r = −0.81, p < 0.05).InterpretationOur results suggest that increased cortical thickness in Alzheimer's disease is relevant to AD symptoms and preferentially occur in brain regions functionally connected to, but anticorrelated with, areas of brain atrophy. Implications for models of compensatory neuroplasticity in response to neurodegeneration are discussed. ANN NEUROL 2024;95:929–940
Author Phan, Tony X.
Drew, William
Fox, Michael D.
Tetreault, Aaron M.
Darby, R. Ryan
Baratono, Sheena
AuthorAffiliation 2 Center for Brain Circuit Therapeutics, Department of Neurology, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA
1 Department of Neurology, Vanderbilt University Medical Center, Nashville, TN
AuthorAffiliation_xml – name: 1 Department of Neurology, Vanderbilt University Medical Center, Nashville, TN
– name: 2 Center for Brain Circuit Therapeutics, Department of Neurology, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA
Author_xml – sequence: 1
  givenname: Tony X.
  orcidid: 0000-0003-4594-7284
  surname: Phan
  fullname: Phan, Tony X.
  organization: Department of Neurology Vanderbilt University Medical Center Nashville TN
– sequence: 2
  givenname: Sheena
  surname: Baratono
  fullname: Baratono, Sheena
  organization: Center for Brain Circuit Therapeutics, Department of Neurology Brigham and Women's Hospital, Harvard Medical School Boston MA
– sequence: 3
  givenname: William
  orcidid: 0000-0002-9178-8731
  surname: Drew
  fullname: Drew, William
  organization: Center for Brain Circuit Therapeutics, Department of Neurology Brigham and Women's Hospital, Harvard Medical School Boston MA
– sequence: 4
  givenname: Aaron M.
  surname: Tetreault
  fullname: Tetreault, Aaron M.
  organization: Department of Neurology Vanderbilt University Medical Center Nashville TN
– sequence: 5
  givenname: Michael D.
  orcidid: 0000-0001-8848-6399
  surname: Fox
  fullname: Fox, Michael D.
  organization: Center for Brain Circuit Therapeutics, Department of Neurology Brigham and Women's Hospital, Harvard Medical School Boston MA
– sequence: 6
  givenname: R. Ryan
  orcidid: 0000-0003-0326-1268
  surname: Darby
  fullname: Darby, R. Ryan
  organization: Department of Neurology Vanderbilt University Medical Center Nashville TN
BackLink https://www.ncbi.nlm.nih.gov/pubmed/38400760$$D View this record in MEDLINE/PubMed
BookMark eNplkUtP5DAQhK0Vq2V4HPgDKBIHlkOg_YjtnNBoFlgkpL3A2XKcDmPI2GBnkODXk-ElYE996K9K1V0bZC3EgITsUDikAOzIBnvIpK7FDzKhFaelZqJeIxPgUpQV5WKdbOR8AwC1pPCLrHMtAJSECeHnwSW0GdtiFtPgne2Ly7l3twFzLnwopv3THP0C034u_vi8QrfIz872Gbff5ia5Oj25nP0tL_6dnc-mF6UTIIayctIKBGyc6qpK8MaiZdg2tuGg6kYppSVI2lpt66buGo1KVi2luqKsYxz4Jjl-9b1bNgtsHYYh2d7cJb-w6dFE683XTfBzcx0fDKUgoWZ8dPj95pDi_RLzYBY-O-x7GzAus-EgtFKUyWpE976hN3GZwnjfCyWZ0oKO1O7nSB9Z3h86AkevgEsx54SdcX6wg4-rhL43FMyqMjNWZl4qGxUH3xTvpv-zzxiZlW4
CitedBy_id crossref_primary_10_1093_brain_awae352
crossref_primary_10_3390_cimb46070407
crossref_primary_10_3390_jpm14090948
crossref_primary_10_1016_j_neuroscience_2024_08_040
crossref_primary_10_1016_j_nicl_2024_103672
crossref_primary_10_1002_hbm_70121
crossref_primary_10_3233_JAD_240368
Cites_doi 10.1093/brain/awx254
10.1002/hbm.22927
10.1212/WNL.0000000000003404
10.1016/j.neuron.2011.08.021
10.1007/978-3-319-24277-4
10.1038/nrn2201
10.1126/science.1215330
10.1093/brain/aww288
10.1038/nature18933
10.1523/JNEUROSCI.5309-07.2008
10.1523/JNEUROSCI.2998-14.2015
10.1001/archneurol.2011.108
10.1038/sdata.2015.31
10.1056/NEJMra1706158
10.1007/s00415-015-7892-3
10.1093/brain/awz007
10.1016/j.dadm.2018.06.002
10.1093/brain/awaa058
10.1016/j.neuron.2009.03.024
10.1016/j.parkreldis.2015.10.013
10.1093/brain/awv191
10.1523/JNEUROSCI.2170-12.2012
10.1093/braincomms/fcac134
10.1186/s13195-020-00595-5
10.1007/s00415-015-7687-6
10.1002/mds.26154
10.1016/j.neurobiolaging.2014.07.005
10.1097/NEN.0b013e3181772794
10.1016/j.neuroimage.2020.117502
10.1002/hbm.26259
10.1093/ons/opy257
10.1093/cercor/bhn113
10.1016/S1474-4422(12)70191-6
10.1016/j.parkreldis.2012.06.003
10.1002/jmri.21049
10.1016/j.neuroimage.2012.02.084
10.1038/s41467-019-11353-z
10.1093/brain/awv228
10.1176/jnp.12.2.233
10.1016/j.neuroimage.2020.117059
10.1016/j.neuroimage.2011.02.076
10.1136/jnnp-2017-315719
10.1093/brain/awx125
10.1016/j.neurobiolaging.2011.06.007
10.1016/j.jalz.2017.09.013
10.3233/JAD-2010-100678
10.1016/j.tics.2013.08.012
10.1001/jamaneurol.2023.0001
10.1016/j.cortex.2011.02.011
10.1002/ana.24186
10.1016/j.ynirp.2021.100066
10.1212/WNL.0000000000200947
10.1093/brain/awl388
10.1212/WNL.57.12.2236
10.2174/1573405054038726
10.1016/j.neuroimage.2017.12.072
10.1016/j.neuroimage.2010.05.041
10.1176/jnp.12.1.25
10.1016/j.nicl.2015.01.017
10.1038/427311a
10.1073/pnas.070039597
10.1073/pnas.1317918110
10.1196/annals.1440.011
10.1093/brain/awy292
10.1093/aje/155.12.1081
10.1073/pnas.1904931116
10.1083/jcb.201709069
10.1016/j.neuroimage.2011.09.015
10.1073/pnas.1814117115
10.1093/brain/awz037
10.1212/WNL.57.11.2117
10.1016/j.neuroimage.2010.09.005
10.1006/nimg.1998.0395
10.1016/j.neuron.2012.03.004
10.1002/hbm.22248
10.1093/brain/awm270
10.1073/pnas.1602413113
10.1016/j.neurobiolaging.2023.05.004
10.1002/ana.25901
10.1093/brain/awu101
10.1073/pnas.1706587115
10.1016/j.nicl.2022.103282
10.1093/brain/awq075
10.1152/jn.00338.2011
ContentType Journal Article
Copyright 2024 The Authors. Annals of Neurology published by Wiley Periodicals LLC on behalf of American Neurological Association.
2024. This article is published under http://creativecommons.org/licenses/by-nc/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
Copyright_xml – notice: 2024 The Authors. Annals of Neurology published by Wiley Periodicals LLC on behalf of American Neurological Association.
– notice: 2024. This article is published under http://creativecommons.org/licenses/by-nc/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
CorporateAuthor For the Alzheimer's Disease Neuroimaging Initiative
for the Alzheimer's Disease Metabolomics Consortium
Alzheimer's Disease Neuroimaging Initiative
Alzheimer's Disease Metabolomics Consortium
CorporateAuthor_xml – name: for the Alzheimer's Disease Metabolomics Consortium
– name: For the Alzheimer's Disease Neuroimaging Initiative
– name: Alzheimer's Disease Neuroimaging Initiative
– name: Alzheimer's Disease Metabolomics Consortium
DBID AAYXX
CITATION
CGR
CUY
CVF
ECM
EIF
NPM
7TK
7U7
C1K
K9.
7X8
5PM
DOI 10.1002/ana.26894
DatabaseName CrossRef
Medline
MEDLINE
MEDLINE (Ovid)
MEDLINE
MEDLINE
PubMed
Neurosciences Abstracts
Toxicology Abstracts
Environmental Sciences and Pollution Management
ProQuest Health & Medical Complete (Alumni)
MEDLINE - Academic
PubMed Central (Full Participant titles)
DatabaseTitle CrossRef
MEDLINE
Medline Complete
MEDLINE with Full Text
PubMed
MEDLINE (Ovid)
ProQuest Health & Medical Complete (Alumni)
Toxicology Abstracts
Neurosciences Abstracts
Environmental Sciences and Pollution Management
MEDLINE - Academic
DatabaseTitleList MEDLINE - Academic
MEDLINE
ProQuest Health & Medical Complete (Alumni)
Database_xml – sequence: 1
  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: 2
  dbid: EIF
  name: MEDLINE
  url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search
  sourceTypes: Index Database
DeliveryMethod fulltext_linktorsrc
Discipline Medicine
EISSN 1531-8249
EndPage 940
ExternalDocumentID PMC11060923
38400760
10_1002_ana_26894
Genre Research Support, U.S. Gov't, Non-P.H.S
Research Support, Non-U.S. Gov't
Journal Article
Research Support, N.I.H., Extramural
GrantInformation_xml – fundername: Alzheimer's Association
– fundername: NIA NIH HHS
  grantid: R56 AG069086
– fundername: NIH HHS
  grantid: 1K23AG070320-01A1
– fundername: NIH HHS
  grantid: R56AG069086
– fundername: NIA NIH HHS
  grantid: K23 AG070320
GroupedDBID ---
.3N
.55
.GA
.GJ
.Y3
05W
0R~
10A
1CY
1L6
1OB
1OC
1ZS
23M
2QL
31~
33P
3O-
3SF
3WU
4.4
4ZD
50Y
50Z
51W
51X
52M
52N
52O
52P
52R
52S
52T
52U
52V
52W
52X
53G
5GY
5VS
66C
6J9
6P2
6PF
702
7PT
8-0
8-1
8-3
8-4
8-5
8UM
930
A01
A03
AAEJM
AAESR
AAEVG
AAHHS
AAHQN
AAIPD
AAMNL
AANHP
AANLZ
AAONW
AAQQT
AASGY
AAWTL
AAXRX
AAYCA
AAYXX
AAZKR
ABCQN
ABCUV
ABEML
ABIJN
ABIVO
ABJNI
ABLJU
ABOCM
ABPVW
ABQWH
ABXGK
ACAHQ
ACBMB
ACBWZ
ACCFJ
ACCZN
ACGFO
ACGFS
ACGOF
ACMXC
ACPOU
ACPRK
ACRPL
ACSCC
ACXBN
ACXQS
ACYXJ
ADBBV
ADBTR
ADEOM
ADIZJ
ADKYN
ADMGS
ADNMO
ADOZA
ADXAS
ADZMN
ADZOD
AEEZP
AEGXH
AEIGN
AEIMD
AENEX
AEQDE
AEUYR
AEYWJ
AFAZI
AFBPY
AFFNX
AFFPM
AFGKR
AFRAH
AFWVQ
AFZJQ
AGHNM
AGQPQ
AGYGG
AHBTC
AHMBA
AI.
AIACR
AIAGR
AITYG
AIURR
AIWBW
AJBDE
AJJEV
ALAGY
ALMA_UNASSIGNED_HOLDINGS
ALUQN
ALVPJ
AMBMR
AMYDB
ASPBG
ATUGU
AVWKF
AZBYB
AZFZN
AZVAB
BAFTC
BDRZF
BFHJK
BHBCM
BMXJE
BROTX
BRXPI
BY8
C45
CITATION
CS3
D-6
D-7
D-E
D-F
DCZOG
DPXWK
DR1
DR2
DRFUL
DRMAN
DRSTM
EBS
EJD
EMOBN
F00
F01
F04
F5P
F8P
FEDTE
FUBAC
FYBCS
G-S
G.N
GNP
GODZA
GOZPB
GRPMH
H.X
HBH
HF~
HGLYW
HHY
HHZ
HVGLF
HZ~
IX1
J0M
J5H
JPC
KBYEO
KD1
KQQ
L7B
LATKE
LAW
LC2
LC3
LEEKS
LH4
LITHE
LOXES
LP6
LP7
LUTES
LW6
LXL
LXN
LXY
LYRES
M6M
MEWTI
MK4
MRFUL
MRMAN
MRSTM
MSFUL
MSMAN
MSSTM
MXFUL
MXMAN
MXSTM
N04
N05
N4W
N9A
NF~
NNB
O66
O9-
OHT
OIG
OVD
P2P
P2W
P2X
P2Z
P4B
P4D
PALCI
PQQKQ
Q.-
Q.N
Q11
QB0
QRW
R.K
RIWAO
RJQFR
ROL
RX1
SAMSI
SJN
SUPJJ
TEORI
UB1
V2E
V8K
V9Y
VH1
W8V
W99
WBKPD
WH7
WHWMO
WIB
WIH
WIJ
WIK
WJL
WOHZO
WQJ
WVDHM
WXI
WXSBR
X7M
XG1
XJT
XPP
XSW
XV2
YOC
YQJ
ZGI
ZRF
ZRR
ZXP
ZZTAW
~IA
~WT
~X8
AAMMB
AEFGJ
AGXDD
AIDQK
AIDYY
CGR
CUY
CVF
ECM
EIF
NPM
7TK
7U7
C1K
K9.
7X8
5PM
ID FETCH-LOGICAL-c404t-5c6a4e0ebc7f5543baea2edbab3079b77786061da8a9b9fb8e765d118512f2303
ISSN 0364-5134
1531-8249
IngestDate Thu Aug 21 18:26:35 EDT 2025
Fri Jul 11 12:29:16 EDT 2025
Fri Jul 25 12:11:41 EDT 2025
Mon Jul 21 05:57:12 EDT 2025
Tue Jul 01 02:24:18 EDT 2025
Thu Apr 24 23:06:35 EDT 2025
IsDoiOpenAccess false
IsOpenAccess true
IsPeerReviewed true
IsScholarly true
Issue 5
Language English
License 2024 The Authors. Annals of Neurology published by Wiley Periodicals LLC on behalf of American Neurological Association.
LinkModel OpenURL
MergedId FETCHMERGED-LOGICAL-c404t-5c6a4e0ebc7f5543baea2edbab3079b77786061da8a9b9fb8e765d118512f2303
Notes ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 14
content type line 23
RRD and MDF contributed to conception and design of the study, acquisition and analysis of data, and drafting a significant portion of the manuscript or figures. TXP, SB, WD, and AMT contributed to acquisition and analysis of data and drafting a significant portion of the manuscript or figures.
Author Contributions
Authors contributed equally to this work
ORCID 0000-0002-9178-8731
0000-0001-8848-6399
0000-0003-0326-1268
0000-0003-4594-7284
OpenAccessLink https://www.ncbi.nlm.nih.gov/pmc/articles/11060923
PMID 38400760
PQID 3048627841
PQPubID 946345
PageCount 12
ParticipantIDs pubmedcentral_primary_oai_pubmedcentral_nih_gov_11060923
proquest_miscellaneous_3048771265
proquest_journals_3048627841
pubmed_primary_38400760
crossref_citationtrail_10_1002_ana_26894
crossref_primary_10_1002_ana_26894
ProviderPackageCode CITATION
AAYXX
PublicationCentury 2000
PublicationDate 2024-05-01
PublicationDateYYYYMMDD 2024-05-01
PublicationDate_xml – month: 05
  year: 2024
  text: 2024-05-01
  day: 01
PublicationDecade 2020
PublicationPlace United States
PublicationPlace_xml – name: United States
– name: Minneapolis
PublicationTitle Annals of neurology
PublicationTitleAlternate Ann Neurol
PublicationYear 2024
Publisher Wiley Subscription Services, Inc
Publisher_xml – name: Wiley Subscription Services, Inc
References e_1_2_9_75_1
e_1_2_9_31_1
e_1_2_9_52_1
e_1_2_9_50_1
e_1_2_9_73_1
e_1_2_9_79_1
e_1_2_9_10_1
e_1_2_9_35_1
e_1_2_9_56_1
e_1_2_9_77_1
e_1_2_9_12_1
e_1_2_9_33_1
e_1_2_9_54_1
e_1_2_9_71_1
Gęsiarz F (e_1_2_9_59_1) 2015; 9
e_1_2_9_14_1
e_1_2_9_39_1
e_1_2_9_16_1
e_1_2_9_37_1
e_1_2_9_58_1
e_1_2_9_64_1
e_1_2_9_87_1
e_1_2_9_20_1
e_1_2_9_62_1
e_1_2_9_89_1
e_1_2_9_22_1
e_1_2_9_45_1
e_1_2_9_68_1
e_1_2_9_83_1
e_1_2_9_24_1
e_1_2_9_43_1
e_1_2_9_66_1
e_1_2_9_85_1
e_1_2_9_8_1
e_1_2_9_6_1
e_1_2_9_81_1
e_1_2_9_4_1
e_1_2_9_60_1
e_1_2_9_2_1
e_1_2_9_26_1
e_1_2_9_49_1
e_1_2_9_28_1
e_1_2_9_47_1
e_1_2_9_30_1
e_1_2_9_53_1
e_1_2_9_74_1
e_1_2_9_51_1
e_1_2_9_72_1
e_1_2_9_11_1
e_1_2_9_34_1
e_1_2_9_57_1
e_1_2_9_78_1
e_1_2_9_13_1
e_1_2_9_32_1
e_1_2_9_55_1
e_1_2_9_76_1
e_1_2_9_70_1
e_1_2_9_15_1
e_1_2_9_38_1
e_1_2_9_17_1
e_1_2_9_36_1
R Core Team (e_1_2_9_41_1) 2020
e_1_2_9_19_1
Monakow C (e_1_2_9_18_1) 1914
e_1_2_9_42_1
e_1_2_9_63_1
e_1_2_9_88_1
e_1_2_9_40_1
e_1_2_9_61_1
e_1_2_9_21_1
e_1_2_9_46_1
e_1_2_9_67_1
e_1_2_9_84_1
e_1_2_9_23_1
e_1_2_9_44_1
e_1_2_9_65_1
e_1_2_9_86_1
e_1_2_9_7_1
e_1_2_9_80_1
e_1_2_9_5_1
e_1_2_9_82_1
e_1_2_9_3_1
e_1_2_9_9_1
e_1_2_9_25_1
e_1_2_9_27_1
e_1_2_9_48_1
e_1_2_9_69_1
e_1_2_9_29_1
References_xml – ident: e_1_2_9_42_1
– ident: e_1_2_9_51_1
  doi: 10.1093/brain/awx254
– ident: e_1_2_9_52_1
  doi: 10.1002/hbm.22927
– volume-title: R: a Language and Environment for Statistical Computing [Internet]
  year: 2020
  ident: e_1_2_9_41_1
– ident: e_1_2_9_28_1
  doi: 10.1212/WNL.0000000000003404
– ident: e_1_2_9_81_1
  doi: 10.1016/j.neuron.2011.08.021
– ident: e_1_2_9_43_1
  doi: 10.1007/978-3-319-24277-4
– ident: e_1_2_9_29_1
  doi: 10.1038/nrn2201
– ident: e_1_2_9_80_1
  doi: 10.1126/science.1215330
– ident: e_1_2_9_24_1
  doi: 10.1093/brain/aww288
– ident: e_1_2_9_44_1
  doi: 10.1038/nature18933
– ident: e_1_2_9_71_1
  doi: 10.1523/JNEUROSCI.5309-07.2008
– ident: e_1_2_9_75_1
  doi: 10.1523/JNEUROSCI.2998-14.2015
– ident: e_1_2_9_33_1
  doi: 10.1001/archneurol.2011.108
– ident: e_1_2_9_54_1
  doi: 10.1038/sdata.2015.31
– ident: e_1_2_9_22_1
  doi: 10.1056/NEJMra1706158
– ident: e_1_2_9_67_1
  doi: 10.1007/s00415-015-7892-3
– ident: e_1_2_9_68_1
  doi: 10.1093/brain/awz007
– ident: e_1_2_9_36_1
  doi: 10.1016/j.dadm.2018.06.002
– ident: e_1_2_9_8_1
  doi: 10.1093/brain/awaa058
– ident: e_1_2_9_3_1
  doi: 10.1016/j.neuron.2009.03.024
– ident: e_1_2_9_15_1
  doi: 10.1016/j.parkreldis.2015.10.013
– ident: e_1_2_9_50_1
  doi: 10.1093/brain/awv191
– ident: e_1_2_9_49_1
  doi: 10.1523/JNEUROSCI.2170-12.2012
– ident: e_1_2_9_85_1
  doi: 10.1093/braincomms/fcac134
– ident: e_1_2_9_37_1
  doi: 10.1186/s13195-020-00595-5
– ident: e_1_2_9_55_1
  doi: 10.1007/s00415-015-7687-6
– ident: e_1_2_9_16_1
  doi: 10.1002/mds.26154
– volume: 9
  start-page: 135
  year: 2015
  ident: e_1_2_9_59_1
  article-title: Goal‐directed, habitual and Pavlovian prosocial behavior
  publication-title: Front Behav Neurosci
– ident: e_1_2_9_65_1
  doi: 10.1016/j.neurobiolaging.2014.07.005
– ident: e_1_2_9_70_1
  doi: 10.1097/NEN.0b013e3181772794
– ident: e_1_2_9_78_1
  doi: 10.1016/j.neuroimage.2020.117502
– ident: e_1_2_9_74_1
  doi: 10.1002/hbm.26259
– ident: e_1_2_9_58_1
  doi: 10.1093/ons/opy257
– ident: e_1_2_9_2_1
  doi: 10.1093/cercor/bhn113
– ident: e_1_2_9_10_1
  doi: 10.1016/S1474-4422(12)70191-6
– ident: e_1_2_9_14_1
  doi: 10.1016/j.parkreldis.2012.06.003
– ident: e_1_2_9_38_1
  doi: 10.1002/jmri.21049
– ident: e_1_2_9_88_1
  doi: 10.1016/j.neuroimage.2012.02.084
– ident: e_1_2_9_7_1
  doi: 10.1038/s41467-019-11353-z
– ident: e_1_2_9_23_1
  doi: 10.1093/brain/awv228
– ident: e_1_2_9_48_1
  doi: 10.1176/jnp.12.2.233
– ident: e_1_2_9_57_1
  doi: 10.1016/j.neuroimage.2020.117059
– ident: e_1_2_9_87_1
  doi: 10.1016/j.neuroimage.2011.02.076
– ident: e_1_2_9_12_1
  doi: 10.1136/jnnp-2017-315719
– ident: e_1_2_9_25_1
  doi: 10.1093/brain/awx125
– ident: e_1_2_9_31_1
  doi: 10.1016/j.neurobiolaging.2011.06.007
– ident: e_1_2_9_83_1
  doi: 10.1016/j.jalz.2017.09.013
– ident: e_1_2_9_56_1
  doi: 10.3233/JAD-2010-100678
– ident: e_1_2_9_11_1
  doi: 10.1016/j.tics.2013.08.012
– ident: e_1_2_9_21_1
  doi: 10.1001/jamaneurol.2023.0001
– ident: e_1_2_9_32_1
  doi: 10.1016/j.cortex.2011.02.011
– ident: e_1_2_9_84_1
  doi: 10.1002/ana.24186
– ident: e_1_2_9_89_1
  doi: 10.1016/j.ynirp.2021.100066
– ident: e_1_2_9_64_1
  doi: 10.1212/WNL.0000000000200947
– ident: e_1_2_9_63_1
  doi: 10.1093/brain/awl388
– ident: e_1_2_9_61_1
  doi: 10.1212/WNL.57.12.2236
– ident: e_1_2_9_72_1
  doi: 10.2174/1573405054038726
– ident: e_1_2_9_46_1
  doi: 10.1016/j.neuroimage.2017.12.072
– ident: e_1_2_9_79_1
  doi: 10.1016/j.neuroimage.2010.05.041
– ident: e_1_2_9_62_1
  doi: 10.1176/jnp.12.1.25
– ident: e_1_2_9_66_1
  doi: 10.1016/j.nicl.2015.01.017
– ident: e_1_2_9_77_1
  doi: 10.1038/427311a
– ident: e_1_2_9_76_1
  doi: 10.1073/pnas.070039597
– ident: e_1_2_9_9_1
  doi: 10.1073/pnas.1317918110
– volume-title: Die Lokalisation im Grosshirn : und der Abbau der Funktion durch kortikale Herde
  year: 1914
  ident: e_1_2_9_18_1
– ident: e_1_2_9_5_1
  doi: 10.1196/annals.1440.011
– ident: e_1_2_9_6_1
  doi: 10.1093/brain/awy292
– ident: e_1_2_9_60_1
  doi: 10.1093/aje/155.12.1081
– ident: e_1_2_9_73_1
  doi: 10.1073/pnas.1904931116
– ident: e_1_2_9_82_1
  doi: 10.1083/jcb.201709069
– ident: e_1_2_9_40_1
  doi: 10.1016/j.neuroimage.2011.09.015
– ident: e_1_2_9_26_1
  doi: 10.1073/pnas.1814117115
– ident: e_1_2_9_13_1
  doi: 10.1093/brain/awz037
– ident: e_1_2_9_47_1
  doi: 10.1212/WNL.57.11.2117
– ident: e_1_2_9_4_1
  doi: 10.1016/j.neuroimage.2010.09.005
– ident: e_1_2_9_39_1
  doi: 10.1006/nimg.1998.0395
– ident: e_1_2_9_19_1
  doi: 10.1016/j.neuron.2012.03.004
– ident: e_1_2_9_34_1
  doi: 10.1002/hbm.22248
– ident: e_1_2_9_69_1
  doi: 10.1093/brain/awm270
– ident: e_1_2_9_45_1
  doi: 10.1073/pnas.1602413113
– ident: e_1_2_9_86_1
  doi: 10.1016/j.neurobiolaging.2023.05.004
– ident: e_1_2_9_20_1
  doi: 10.1002/ana.25901
– ident: e_1_2_9_17_1
  doi: 10.1093/brain/awu101
– ident: e_1_2_9_27_1
  doi: 10.1073/pnas.1706587115
– ident: e_1_2_9_35_1
  doi: 10.1016/j.nicl.2022.103282
– ident: e_1_2_9_30_1
  doi: 10.1093/brain/awq075
– ident: e_1_2_9_53_1
  doi: 10.1152/jn.00338.2011
SSID ssj0009610
Score 2.4890015
Snippet Patients with Alzheimer's disease (AD) have diffuse brain atrophy, but some regions, such as the anterior cingulate cortex (ACC), are spared and may even show...
ObjectivePatients with Alzheimer's disease (AD) have diffuse brain atrophy, but some regions, such as the anterior cingulate cortex (ACC), are spared and may...
SourceID pubmedcentral
proquest
pubmed
crossref
SourceType Open Access Repository
Aggregation Database
Index Database
Enrichment Source
StartPage 929
SubjectTerms Aged
Aged, 80 and over
Alzheimer Disease - diagnostic imaging
Alzheimer Disease - pathology
Alzheimer's disease
Atrophy
Atrophy - pathology
Brain
Brain Cortical Thickness
Brain mapping
Cerebral Cortex - diagnostic imaging
Cerebral Cortex - pathology
Cognitive ability
Cortex (cingulate)
Cross-Sectional Studies
Dementia disorders
Female
Frontotemporal dementia
Gyrus Cinguli - diagnostic imaging
Gyrus Cinguli - pathology
Humans
Magnetic Resonance Imaging
Male
Medical imaging
Middle Aged
Neurodegenerative diseases
Neuroimaging
Neuroplasticity
Signs and symptoms
Thickness
Visual cortex
Title Increased Cortical Thickness in Alzheimer's Disease
URI https://www.ncbi.nlm.nih.gov/pubmed/38400760
https://www.proquest.com/docview/3048627841
https://www.proquest.com/docview/3048771265
https://pubmed.ncbi.nlm.nih.gov/PMC11060923
Volume 95
hasFullText 1
inHoldings 1
isFullTextHit
isPrint
link http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV3di9QwEA96gvgifls9pYqgcPRs0zQfj6J3HHJ7inZh30rSZtnFpSv78eD99U4-mnbdQ05fytKGbMlMpvObmfwGoTdZzlTBdZ5QThUAFMYSSQClFFIyMaWNru0hsdEFPRuTz5Ni0peN2dMlG3VcX155ruR_pAr3QK7mlOw_SDZMCjfgN8gXriBhuF5LxrC5TU25CdIuVy4oXc7m9Q9rvkwgY3E503PbH4WtDdFmyMXs0SdbXsthhP3rzDcuXra_jiZ9wNOk5W277qPvM8DAwap_WmmbJfIBnBAR0KaUfbtw7AZyBco2GkYaMOnr-q5pzwa2K6ckKTIfp9Sdbc0Sjh1DaWd8XYdNr2TFwJIKHwhxH2XhOJ327L3jj5WtPMaUC9J_1LpE_sWX6nR8fl6VJ5PyJrqFAUxY4P2tJxkT1HJWhFfu-KdS_D5MvOu17EGRPytqBy5KeQ_d9dgi_uAU5T66odsH6PbIV088RHnQl7jTlzjoSzxv46Avb9ex15ZHaHx6Un48S3zTjKQmKdkkRU0l0alWNZuCq5grqSXWjZIKrLlQzPAFgg_XSC6FElPFNaNFAzATPL8p4NH8MTpol61-iuIGvLeaYIYBhZEMK8Fl3miVNjC9kJJH6F23KFXtGeVNY5NF5biwcQXrV9n1i9DrMPSno1G5atBht7KV32XrKjeckDY7HqFX4THYQJPYkq1ebt0YxjJMiwg9cYII_5JzYrPPEeI7IgoDDL_67pN2PrM86-AZ0xQA0LO_v9dzdKffLYfoYLPa6hfgqW7US6tovwETaJVe
linkProvider Wiley-Blackwell
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=Increased+Cortical+Thickness+in+Alzheimer%27s+Disease&rft.jtitle=Annals+of+neurology&rft.au=Phan%2C+Tony+X&rft.au=Baratono%2C+Sheena&rft.au=Drew%2C+William&rft.au=Tetreault%2C+Aaron+M&rft.date=2024-05-01&rft.pub=Wiley+Subscription+Services%2C+Inc&rft.issn=0364-5134&rft.eissn=1531-8249&rft.volume=95&rft.issue=5&rft.spage=929&rft.epage=940&rft_id=info:doi/10.1002%2Fana.26894&rft.externalDBID=NO_FULL_TEXT
thumbnail_l http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=0364-5134&client=summon
thumbnail_m http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=0364-5134&client=summon
thumbnail_s http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=0364-5134&client=summon