Cognitive and Anatomic Contributions of Metabolic Decline in Alzheimer Disease and Cerebrovascular Disease

BACKGROUND Alzheimer disease and cerebrovascular disease affect elderly persons through alterations in brain structure and metabolism that produce cognitive decline. Understanding how each disease contributes to dementia is essential from both a pathophysiologic and diagnostic perspective. OBJECTIVE...

Full description

Saved in:
Bibliographic Details
Published inArchives of neurology (Chicago) Vol. 65; no. 5; pp. 650 - 655
Main Authors Kuczynski, Beth, Reed, Bruce, Mungas, Dan, Weiner, Michael, Chui, Helena C, Jagust, William
Format Journal Article
LanguageEnglish
Published Chicago, IL American Medical Association 01.05.2008
Subjects
Online AccessGet full text
ISSN0003-9942
2168-6149
1538-3687
1538-3687
2168-6157
DOI10.1001/archneur.65.5.650

Cover

Abstract BACKGROUND Alzheimer disease and cerebrovascular disease affect elderly persons through alterations in brain structure and metabolism that produce cognitive decline. Understanding how each disease contributes to dementia is essential from both a pathophysiologic and diagnostic perspective. OBJECTIVE To elucidate how baseline cognitive function (episodic memory and executive function) and brain anatomy (white matter hyperintensities and hippocampal volume) are associated with baseline (positron emission tomography-1 [PET1]) and longitudinal (PET2) glucose metabolism in 38 subjects older than 55 years ranging from normal cognition, cognitive impairment without dementia, and dementia. DESIGN Cross-sectional regression analyses across subjects. SETTING Multicenter, university-based study of subcortical vascular dementia. MAIN OUTCOME MEASURES Regional cerebral glucose metabolism was the primary outcome, with the major hypotheses that memory and hippocampal volume are related to temporoparietal hypometabolism while executive function and white matter hyperintensities correlate with frontal lobe hypometabolism. RESULTS Low baseline hippocampal volume predicted longitudinal development (PET2) of medial temporal hypometabolism. Lower memory was associated with parietal and cingulate hypometabolism at PET1, which increased at the 2-year-follow-up (PET2). Executive function was associated with frontal and temporoparietal hypometabolism at PET1 but only with frontal hypometabolism at follow-up. White matter hyperintensities predicted hypometabolism over time in the frontoparietal regions, predicting a rate of metabolic change (PET1 − PET2/time). CONCLUSIONS Low baseline episodic memory and hippocampal volume predict the metabolic alterations associated with Alzheimer disease, whereas elevated baseline white matter hyperintensities predict a different pattern of metabolic decline that is plausibly associated with cerebrovascular disease.Arch Neurol. 2008;65(5):650-655-->
AbstractList Alzheimer disease and cerebrovascular disease affect elderly persons through alterations in brain structure and metabolism that produce cognitive decline. Understanding how each disease contributes to dementia is essential from both a pathophysiologic and diagnostic perspective.BACKGROUNDAlzheimer disease and cerebrovascular disease affect elderly persons through alterations in brain structure and metabolism that produce cognitive decline. Understanding how each disease contributes to dementia is essential from both a pathophysiologic and diagnostic perspective.To elucidate how baseline cognitive function (episodic memory and executive function) and brain anatomy (white matter hyperintensities and hippocampal volume) are associated with baseline (positron emission tomography-1 [PET1]) and longitudinal (PET2) glucose metabolism in 38 subjects older than 55 years ranging from normal cognition, cognitive impairment without dementia, and dementia.OBJECTIVETo elucidate how baseline cognitive function (episodic memory and executive function) and brain anatomy (white matter hyperintensities and hippocampal volume) are associated with baseline (positron emission tomography-1 [PET1]) and longitudinal (PET2) glucose metabolism in 38 subjects older than 55 years ranging from normal cognition, cognitive impairment without dementia, and dementia.Cross-sectional regression analyses across subjects.DESIGNCross-sectional regression analyses across subjects.Multicenter, university-based study of subcortical vascular dementia.SETTINGMulticenter, university-based study of subcortical vascular dementia.Regional cerebral glucose metabolism was the primary outcome, with the major hypotheses that memory and hippocampal volume are related to temporoparietal hypometabolism while executive function and white matter hyperintensities correlate with frontal lobe hypometabolism.MAIN OUTCOME MEASURESRegional cerebral glucose metabolism was the primary outcome, with the major hypotheses that memory and hippocampal volume are related to temporoparietal hypometabolism while executive function and white matter hyperintensities correlate with frontal lobe hypometabolism.Low baseline hippocampal volume predicted longitudinal development (PET2) of medial temporal hypometabolism. Lower memory was associated with parietal and cingulate hypometabolism at PET1, which increased at the 2-year-follow-up (PET2). Executive function was associated with frontal and temporoparietal hypometabolism at PET1 but only with frontal hypometabolism at follow-up. White matter hyperintensities predicted hypometabolism over time in the frontoparietal regions, predicting a rate of metabolic change (PET1 - PET2/time).RESULTSLow baseline hippocampal volume predicted longitudinal development (PET2) of medial temporal hypometabolism. Lower memory was associated with parietal and cingulate hypometabolism at PET1, which increased at the 2-year-follow-up (PET2). Executive function was associated with frontal and temporoparietal hypometabolism at PET1 but only with frontal hypometabolism at follow-up. White matter hyperintensities predicted hypometabolism over time in the frontoparietal regions, predicting a rate of metabolic change (PET1 - PET2/time).Low baseline episodic memory and hippocampal volume predict the metabolic alterations associated with Alzheimer disease, whereas elevated baseline white matter hyperintensities predict a different pattern of metabolic decline that is plausibly associated with cerebrovascular disease.CONCLUSIONSLow baseline episodic memory and hippocampal volume predict the metabolic alterations associated with Alzheimer disease, whereas elevated baseline white matter hyperintensities predict a different pattern of metabolic decline that is plausibly associated with cerebrovascular disease.
BACKGROUND Alzheimer disease and cerebrovascular disease affect elderly persons through alterations in brain structure and metabolism that produce cognitive decline. Understanding how each disease contributes to dementia is essential from both a pathophysiologic and diagnostic perspective. OBJECTIVE To elucidate how baseline cognitive function (episodic memory and executive function) and brain anatomy (white matter hyperintensities and hippocampal volume) are associated with baseline (positron emission tomography-1 [PET1]) and longitudinal (PET2) glucose metabolism in 38 subjects older than 55 years ranging from normal cognition, cognitive impairment without dementia, and dementia. DESIGN Cross-sectional regression analyses across subjects. SETTING Multicenter, university-based study of subcortical vascular dementia. MAIN OUTCOME MEASURES Regional cerebral glucose metabolism was the primary outcome, with the major hypotheses that memory and hippocampal volume are related to temporoparietal hypometabolism while executive function and white matter hyperintensities correlate with frontal lobe hypometabolism. RESULTS Low baseline hippocampal volume predicted longitudinal development (PET2) of medial temporal hypometabolism. Lower memory was associated with parietal and cingulate hypometabolism at PET1, which increased at the 2-year-follow-up (PET2). Executive function was associated with frontal and temporoparietal hypometabolism at PET1 but only with frontal hypometabolism at follow-up. White matter hyperintensities predicted hypometabolism over time in the frontoparietal regions, predicting a rate of metabolic change (PET1 − PET2/time). CONCLUSIONS Low baseline episodic memory and hippocampal volume predict the metabolic alterations associated with Alzheimer disease, whereas elevated baseline white matter hyperintensities predict a different pattern of metabolic decline that is plausibly associated with cerebrovascular disease.Arch Neurol. 2008;65(5):650-655-->
Alzheimer disease and cerebrovascular disease affect elderly persons through alterations in brain structure and metabolism that produce cognitive decline. Understanding how each disease contributes to dementia is essential from both a pathophysiologic and diagnostic perspective. To elucidate how baseline cognitive function (episodic memory and executive function) and brain anatomy (white matter hyperintensities and hippocampal volume) are associated with baseline (positron emission tomography-1 [PET1]) and longitudinal (PET2) glucose metabolism in 38 subjects older than 55 years ranging from normal cognition, cognitive impairment without dementia, and dementia. Cross-sectional regression analyses across subjects. Multicenter, university-based study of subcortical vascular dementia. Regional cerebral glucose metabolism was the primary outcome, with the major hypotheses that memory and hippocampal volume are related to temporoparietal hypometabolism while executive function and white matter hyperintensities correlate with frontal lobe hypometabolism. Low baseline hippocampal volume predicted longitudinal development (PET2) of medial temporal hypometabolism. Lower memory was associated with parietal and cingulate hypometabolism at PET1, which increased at the 2-year-follow-up (PET2). Executive function was associated with frontal and temporoparietal hypometabolism at PET1 but only with frontal hypometabolism at follow-up. White matter hyperintensities predicted hypometabolism over time in the frontoparietal regions, predicting a rate of metabolic change (PET1 - PET2/time). Low baseline episodic memory and hippocampal volume predict the metabolic alterations associated with Alzheimer disease, whereas elevated baseline white matter hyperintensities predict a different pattern of metabolic decline that is plausibly associated with cerebrovascular disease.
Alzheimer disease and cerebrovascular disease affect elderly persons through alterations in brain structure and metabolism that produce cognitive decline. Understanding how each disease contributes to dementia is essential from both a pathophysiologic and diagnostic perspective. To elucidate how baseline cognitive function (episodic memory and executive function) and brain anatomy (white matter hyperintensities and hippocampal volume) are associated with baseline (positron emission tomography-1 [PET1]) and longitudinal (PET2) glucose metabolism in 38 subjects older than 55 years ranging from normal cognition, cognitive impairment without dementia, and dementia. Cross-sectional regression analyses across subjects. Multicenter, university-based study of subcortical vascular dementia. Regional cerebral glucose metabolism was the primary outcome, with the major hypotheses that memory and hippocampal volume are related to temporoparietal hypometabolism while executive function and white matter hyperintensities correlate with frontal lobe hypometabolism. Low baseline hippocampal volume predicted longitudinal development (PET2) of medial temporal hypometabolism. Lower memory was associated with parietal and cingulate hypometabolism at PET1, which increased at the 2-year-follow-up (PET2). Executive function was associated with frontal and temporoparietal hypometabolism at PET1 but only with frontal hypometabolism at follow-up. White matter hyperintensities predicted hypometabolism over time in the frontoparietal regions, predicting a rate of metabolic change (PET1 - PET2/time). Low baseline episodic memory and hippocampal volume predict the metabolic alterations associated with Alzheimer disease, whereas elevated baseline white matter hyperintensities predict a different pattern of metabolic decline that is plausibly associated with cerebrovascular disease.
Author Chui, Helena C
Mungas, Dan
Jagust, William
Kuczynski, Beth
Reed, Bruce
Weiner, Michael
AuthorAffiliation Helen Wills Neuroscience Institute and the Lawrence Berkeley National Laboratory, University of California, Berkeley (Drs Kuczynski and Jagust); Alzheimer's Disease Center, University of California, Davis, and Northern California Veterans Affairs Health Care System, Sacramento (Drs Reed and Mungas); Department of Veterans Affairs Medical Center, University of California, San Francisco (Dr Weiner); and Department of Neurology, University of Southern California, Los Angeles (Dr Chui)
AuthorAffiliation_xml – name: Helen Wills Neuroscience Institute and the Lawrence Berkeley National Laboratory, University of California, Berkeley (Drs Kuczynski and Jagust); Alzheimer's Disease Center, University of California, Davis, and Northern California Veterans Affairs Health Care System, Sacramento (Drs Reed and Mungas); Department of Veterans Affairs Medical Center, University of California, San Francisco (Dr Weiner); and Department of Neurology, University of Southern California, Los Angeles (Dr Chui)
Author_xml – sequence: 1
  givenname: Beth
  surname: Kuczynski
  fullname: Kuczynski, Beth
– sequence: 2
  givenname: Bruce
  surname: Reed
  fullname: Reed, Bruce
– sequence: 3
  givenname: Dan
  surname: Mungas
  fullname: Mungas, Dan
– sequence: 4
  givenname: Michael
  surname: Weiner
  fullname: Weiner, Michael
– sequence: 5
  givenname: Helena C
  surname: Chui
  fullname: Chui, Helena C
– sequence: 6
  givenname: William
  surname: Jagust
  fullname: Jagust, William
BackLink http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20320217$$DView record in Pascal Francis
https://www.ncbi.nlm.nih.gov/pubmed/18474742$$D View this record in MEDLINE/PubMed
BookMark eNp9Uk1r3DAQFSWl2aT9AbkUU2hu3kqyZcmXwuKkH5DSS3sWY62c1SJLqWQvtL--s-xm2-ZQBCPQvPfmjWYuyFmIwRJyxeiSUcreQTKbYOe0bMRSYKDPyIKJSpVVo-QZWVBKq7Jta35OLnLeIoUr1b4g50zVEg9fkG0X74Ob3M4WENbFKsAUR2eKLoYpuX6eXAy5iEPxxU7QR4-pG2u8C7ZwoVj5XxvrRpuKG5ct5INIZ5PtU9xBNrOHU-4leT6Az_bV8b4k3z_cfus-lXdfP37uVncl1JJPZWMGyXuMraqYWvdN3cAajbcSmGCcMamEsfgoh6pvqVQNZ4pS0TJeV31dVZfk_UH3Ye5HuzYWOwGvH5IbIf3UEZz-NxPcRt_HneZCoBZHgeujQIo_ZpsnPbpsrPcQbJyzblpOK_SDwDdPgNs4p4DNaY6GFJeKIej133ZOPh5ngIC3RwB-GPghQTAun3BYi1PO9tXYAWdSzDnZ4Y8U1ft90I_7oBuhBQaKHPmEY9wE-6Fi587_l3l1YMIIp0KyFULS6jdEx8Vt
CODEN ARNEAS
CitedBy_id crossref_primary_10_1016_j_jocn_2011_12_031
crossref_primary_10_1093_brain_awr139
crossref_primary_10_1016_j_jalz_2016_06_2358
crossref_primary_10_1016_j_neuroscience_2011_05_032
crossref_primary_10_1161_STROKEAHA_120_032905
crossref_primary_10_1007_s13311_020_00874_x
crossref_primary_10_3233_JAD_200676
crossref_primary_10_1016_j_neuint_2015_12_001
crossref_primary_10_1038_nrneurol_2011_21
crossref_primary_10_1007_s00702_017_1734_7
crossref_primary_10_1002_hipo_20952
crossref_primary_10_1007_s00259_018_4035_y
crossref_primary_10_3389_fnins_2023_1211044
crossref_primary_10_1097_WNP_0000000000000060
crossref_primary_10_1097_WNP_0b013e3182767d15
crossref_primary_10_1053_j_semnuclmed_2015_09_003
crossref_primary_10_1186_alzrt52
crossref_primary_10_1111_j_1471_4159_2009_06511_x
crossref_primary_10_1017_S1355617710001426
crossref_primary_10_1007_s11064_010_0378_x
crossref_primary_10_1016_j_jns_2010_08_040
crossref_primary_10_1371_journal_pone_0024293
crossref_primary_10_1212_WNL_0b013e31826c1b9d
crossref_primary_10_2967_jnumed_117_190082
crossref_primary_10_1148_rg_343135065
crossref_primary_10_3389_fnagi_2022_841942
crossref_primary_10_1002_jnr_23925
crossref_primary_10_1007_s40336_013_0026_y
crossref_primary_10_1016_j_jalz_2009_04_1228
crossref_primary_10_1177_1533317512470207
crossref_primary_10_3389_fnagi_2021_735334
crossref_primary_10_1016_j_neuroimage_2014_06_060
ContentType Journal Article
Copyright 2008 INIST-CNRS
Copyright American Medical Association May 2008
Copyright_xml – notice: 2008 INIST-CNRS
– notice: Copyright American Medical Association May 2008
DBID AAYXX
CITATION
IQODW
CGR
CUY
CVF
ECM
EIF
NPM
7TK
7U7
C1K
K9.
NAPCQ
7X8
5PM
DOI 10.1001/archneur.65.5.650
DatabaseName CrossRef
Pascal-Francis
Medline
MEDLINE
MEDLINE (Ovid)
MEDLINE
MEDLINE
PubMed
Neurosciences Abstracts
Toxicology Abstracts
Environmental Sciences and Pollution Management
ProQuest Health & Medical Complete (Alumni)
Nursing & Allied Health Premium
MEDLINE - Academic
PubMed Central (Full Participant titles)
DatabaseTitle CrossRef
MEDLINE
Medline Complete
MEDLINE with Full Text
PubMed
MEDLINE (Ovid)
ProQuest Health & Medical Complete (Alumni)
Nursing & Allied Health Premium
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 1538-3687
2168-6157
EndPage 655
ExternalDocumentID PMC2556212
1482179211
18474742
20320217
10_1001_archneur_65_5_650
795570
Genre Multicenter Study
Journal Article
Research Support, N.I.H., Extramural
Feature
GrantInformation_xml – fundername: NIA NIH HHS
  grantid: P30 AG010129
– fundername: NIA NIH HHS
  grantid: AG12435
– fundername: NIA NIH HHS
  grantid: P01 AG012435
GroupedDBID ---
-QF
.55
.GJ
.XZ
23N
2WC
354
39C
4.4
53G
5GY
6J9
AAWTL
ABCQX
ABJNI
ABOCM
ACGFO
ACGFS
ADBBV
AFFNX
AFOSN
ALMA_UNASSIGNED_HOLDINGS
AMJDE
ARBJA
BAWUL
BRYMA
C1A
C45
CS3
E3Z
EAM
EBS
EJD
EMOBN
EX3
F5P
GX1
L7B
MJL
N4W
N9A
OB2
OBH
OHH
OVD
P2P
RAJ
RXW
SJN
SV3
TEORI
TWZ
VVN
WH7
WOW
X6Y
X7M
XHN
YOC
ZA5
ZY1
AAYXX
CITATION
1CY
2CT
3O-
41~
AAYJJ
ACBNA
ADXHL
AFHKK
H13
H~9
IQODW
RWL
TAE
XJT
XOL
ZGI
ZKB
ZXP
CGR
CUY
CVF
ECM
EIF
NPM
7TK
7U7
C1K
K9.
NAPCQ
7X8
5PM
ID FETCH-LOGICAL-a472t-6cf72b6cf98318db646ad12897a151211785ce46a7f3b9078621800591243b433
ISSN 0003-9942
2168-6149
1538-3687
IngestDate Thu Aug 21 18:25:21 EDT 2025
Fri Sep 05 05:49:55 EDT 2025
Mon Jun 30 16:46:28 EDT 2025
Fri May 30 11:01:45 EDT 2025
Mon Jul 21 09:13:28 EDT 2025
Tue Jul 01 02:14:14 EDT 2025
Thu Apr 24 23:05:54 EDT 2025
Fri Jul 05 02:03:46 EDT 2024
IsDoiOpenAccess false
IsOpenAccess true
IsPeerReviewed false
IsScholarly false
Issue 5
Keywords Nervous system diseases
Alzheimer disease
Central nervous system disease
Metabolic diseases
Degenerative disease
Cerebrovascular disease
Cerebral disorder
Language English
License CC BY 4.0
LinkModel OpenURL
MergedId FETCHMERGED-LOGICAL-a472t-6cf72b6cf98318db646ad12897a151211785ce46a7f3b9078621800591243b433
Notes SourceType-Scholarly Journals-1
ObjectType-Feature-1
content type line 14
ObjectType-Article-1
ObjectType-Feature-2
content type line 23
Author Contributions: Study concept and design: Kuczynski, Reed, Mungas, and Jagust. Acquisition of data: Kuczynski, Reed, Mungas, Weiner, Chui, and Jagust. Analysis and interpretation of data: Kuczynski, Reed, Mungas, and Jagust. Drafting of the manuscript: Kuczynski. Critical revision of the manuscript for important intellectual content: Reed, Mungas, Weiner, Chui, and Jagust. Statistical analysis: Kuczynski, Reed, and Mungas. Obtained funding: Kuczynski, Reed, Mungas, and Jagust. Administrative, technical, and material support: Reed, Weiner, Chui, and Jagust. Study supervision: Jagust.
OpenAccessLink https://doi.org/10.1001/archneur.65.5.650
PMID 18474742
PQID 205982781
PQPubID 42446
PageCount 6
ParticipantIDs pubmedcentral_primary_oai_pubmedcentral_nih_gov_2556212
proquest_miscellaneous_69203897
proquest_journals_205982781
pubmed_primary_18474742
pascalfrancis_primary_20320217
crossref_primary_10_1001_archneur_65_5_650
crossref_citationtrail_10_1001_archneur_65_5_650
ama_primary_795570
ProviderPackageCode CITATION
AAYXX
PublicationCentury 2000
PublicationDate 2008-05-01
PublicationDateYYYYMMDD 2008-05-01
PublicationDate_xml – month: 05
  year: 2008
  text: 2008-05-01
  day: 01
PublicationDecade 2000
PublicationPlace Chicago, IL
PublicationPlace_xml – name: Chicago, IL
– name: United States
– name: Chicago
PublicationTitle Archives of neurology (Chicago)
PublicationTitleAlternate Arch Neurol
PublicationYear 2008
Publisher American Medical Association
Publisher_xml – name: American Medical Association
SSID ssj0012889
Score 1.7194085
Snippet BACKGROUND Alzheimer disease and cerebrovascular disease affect elderly persons through alterations in brain structure and metabolism that produce cognitive...
Alzheimer disease and cerebrovascular disease affect elderly persons through alterations in brain structure and metabolism that produce cognitive decline....
SourceID pubmedcentral
proquest
pubmed
pascalfrancis
crossref
ama
SourceType Open Access Repository
Aggregation Database
Index Database
Enrichment Source
Publisher
StartPage 650
SubjectTerms Aged
Aged, 80 and over
Alzheimer Disease - diagnostic imaging
Alzheimer Disease - metabolism
Alzheimer Disease - pathology
Alzheimer's disease
Atrophy - diagnostic imaging
Atrophy - metabolism
Atrophy - pathology
Biological and medical sciences
Brain
Brain - diagnostic imaging
Brain - metabolism
Brain - pathology
Brain Diseases, Metabolic - diagnostic imaging
Brain Diseases, Metabolic - metabolism
Brain Diseases, Metabolic - pathology
Brain Mapping
Cognition & reasoning
Cognition Disorders - diagnostic imaging
Cognition Disorders - metabolism
Cognition Disorders - pathology
Cross-Sectional Studies
Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases
Dementia, Vascular - diagnostic imaging
Dementia, Vascular - metabolism
Dementia, Vascular - pathology
Disease Progression
Energy Metabolism - physiology
Female
Geriatrics
Glucose - metabolism
Hippocampus - diagnostic imaging
Hippocampus - metabolism
Hippocampus - pathology
Humans
Male
Medical sciences
Memory Disorders - diagnostic imaging
Memory Disorders - metabolism
Memory Disorders - pathology
Nerve Fibers, Myelinated - metabolism
Nerve Fibers, Myelinated - pathology
Neurology
Neuropsychological Tests
Older people
Original Contribution
Positron-Emission Tomography
Predictive Value of Tests
Regression analysis
Studies
Title Cognitive and Anatomic Contributions of Metabolic Decline in Alzheimer Disease and Cerebrovascular Disease
URI http://dx.doi.org/10.1001/archneur.65.5.650
https://www.ncbi.nlm.nih.gov/pubmed/18474742
https://www.proquest.com/docview/205982781
https://www.proquest.com/docview/69203897
https://pubmed.ncbi.nlm.nih.gov/PMC2556212
Volume 65
hasFullText 1
inHoldings 1
isFullTextHit
isPrint
journalDatabaseRights – providerCode: PRVFQY
  databaseName: GFMER Free Medical Journals
  customDbUrl:
  eissn: 1538-3687
  dateEnd: 99991231
  omitProxy: true
  ssIdentifier: ssj0012889
  issn: 0003-9942
  databaseCode: GX1
  dateStart: 0
  isFulltext: true
  titleUrlDefault: http://www.gfmer.ch/Medical_journals/Free_medical.php
  providerName: Geneva Foundation for Medical Education and Research
link http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV3fb9MwELbKkBASQoyfZTDygHhASmkcx3YeR7sxwTpeOtE3y0kdraikpWsf6B_I38Vd7KRJW02AKlmVHVuJ74tz5zt_R8jbCDCRilj6kunQZyzJ4JXSY19oE4uM8TRJ8Lzz4JKfX7HPo2jUav2uRS2tlkknXe89V_I_UoU6kCuekv0HyVaDQgX8B_lCCRKG8q9k3Ktif3D7-yQHAxpD3ZFxqsxjZWNczBJkjXTWfZMWeiXuckzX12bywyyQgROdNMUgPbMAK3kToNqvOXD2kNUWdJgFixN6g21YR21z4csqXf8qU2N_tMFj1r9jzC60BrDw2PNl_Q1mv5mJO5NTj_Av9ynkJiqwdjSg5oDahl-x5tGAS7BmLYtpx9TrLI91uWjbBBMOnFFtBeaWx3bny2AzEuDigTPT4VEn6rhrmyzcl1_V2dXFhRqejobNVms0MQlWXAx287v5Tx-zl6GX36VyuUPuUsE5ZtL4NKpCjUAFKFIxVg9Xete7wYedG6oz_jot6cEcZK6nmc20ss8U2o7oralIw0fkobNtvBML1EPSMvljcm_gojeekO8VXj2Amlfi1Wvg1ZtlXoVXz-HVm-RehVfPYbIYZAuvZdtTcnV2Ouyd-y7Xh6-ZoEufp5mgCZSxhK_MOOGM6zFMXCw06qRBIGSUGqgUWZjEoNdy0E3x5DTop2HCwvAZOchnuXlBvJCZiOoslIZrJrthQjOuaZhyDaaKprJNDmGG1dyyuSgRIwtdm3TLCVepY8fHJC1TZXm9A1VKSvFIRVBAl_dVl3KwWy4-bkix6kG7IcV9gTY5KsWq3BJzA43Irylk0CZvqlZY_9Gpp3MzW90oHlPkyIT-zy0ENvcCiif8aJuIBjiqC5BZvtmST64LhnnkJQSd9uWt93RE7m_e81fkYLlYmdegoS-T4wL-fwAIy-yp
linkProvider Geneva Foundation for Medical Education and Research
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=Cognitive+and+Anatomic+Contributions+of+Metabolic+Decline+in+Alzheimer+Disease+and+Cerebrovascular+Disease&rft.jtitle=Archives+of+neurology+%28Chicago%29&rft.au=Kuczynski%2C+Beth&rft.au=Reed%2C+Bruce&rft.au=Mungas%2C+Dan&rft.au=Weiner%2C+Michael&rft.date=2008-05-01&rft.pub=American+Medical+Association&rft.issn=2168-6149&rft.eissn=2168-6157&rft.volume=65&rft.issue=5&rft.spage=650&rft_id=info:doi/10.1001%2Farchneur.65.5.650&rft.externalDBID=NO_FULL_TEXT&rft.externalDocID=1482179211
thumbnail_l http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=0003-9942&client=summon
thumbnail_m http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=0003-9942&client=summon
thumbnail_s http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=0003-9942&client=summon