Evidence map›Paper›PMID 35414420›Full record

ArticleNeurobiology of aging2022

The canonical pattern of Alzheimer's disease atrophy is linked to white matter hyperintensities in normal controls, differently in normal controls compared to in AD.

Joost M Riphagen, Mahanand Belathur Suresh, David H Salat, Alzheimer's Disease Neuroimaging Initiative (ADNI)

Open access · greenAbstract read
In one paragraph

Article in Neurobiology of aging, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.0field-weighted citation impact, top 26% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 2 countries.

Joost M RiphagenAthinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Harvard Medical, School, Charlestown, MA, USA; Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA; Department of Psychiatry & Neuropsychology, Maastricht University, School for Mental Health & Neuroscience, Alzheimer Center Limburg, Maastricht, the Netherlands. Electronic address: jriph@yahoo.co.uk.
Mahanand Belathur SureshAthinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Harvard Medical, School, Charlestown, MA, USA; Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA; Department of Information Science and Engineering, Sri Jayachamarajendra College of Engineering, Mysuru, India.
David H SalatAthinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Harvard Medical, School, Charlestown, MA, USA; Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA; Neuroimaging Research for Veterans Center, VA Boston Healthcare System, Boston, MA, USA.
Alzheimer's Disease Neuroimaging Initiative (ADNI)
Harvard University · US

Funding

Alzheimer's Disease Neuroimaging Initiative - SupplementU01AG024904 · NIA · NORTHERN CALIFORNIA INSTITUTE RES &EDUC · PI WEINER, MICHAEL W · 2004 to 2015
$121.0M
ULTRAHIGH FIELD TECHNOLOGY FOR FUNCTIONAL IMAGINGP41RR014075 · NCRR · MASSACHUSETTS GENERAL HOSPITAL · PI BOAS, DAVID A · 1999 to 2011
$16.4M
Neuroimaging Biomarkers for disease-modyfying therapies in Hintington's diseaseP01NS058793 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI HERSCH, STEVEN M · 2008 to 2012
$6.6M
Prospective Neuroimaging in Huntington's DiseaseR01NS042861 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI ROSAS, HERMINIA DIANA · 2003 to 2013
$5.6M
Cerebrovascular Contributions to Brain Aging and DementiaR01NR010827 · NINR · MASSACHUSETTS GENERAL HOSPITAL · PI SALAT, DAVID H · 2007 to 2017
$5.0M
Understanding the Contribution of Altered Cerebrovascular Function to the Pathology and Clinical Symptoms of Huntington DiseaseR01NS114562 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI HERMINIA Diana ROSAS · 2021 to 2026
$3.3M
A Storage Area Network for Structural and Functional Image AnalysisS10RR023401 · NCRR · MASSACHUSETTS GENERAL HOSPITAL · PI FISCHL, BRUCE · 2009 to 2009
$2.0M
SILICON GRAPHICS PRISM EXTREME 128P/1TBS10RR023043 · NCRR · MASSACHUSETTS GENERAL HOSPITAL · PI SORENSEN, ALMA GREGORY · 2006 to 2006
$1.5M
Prospective Neuroimaging in Huntington's DiseaseR56NS042861 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI ROSAS, HERMINIA DIANA · 2014 to 2014
$870k
A Siemens MAGNETOTOM Trio 3 Tesla MRI SystemS10RR021110 · NCRR · MASSACHUSETTS GENERAL HOSPITAL · PI ROSEN, BRUCE R · 2006 to 2006
$500k
A 3.0 Tesla MRI System in a Neuroscience ICUS10RR019254 · NCRR · MASSACHUSETTS GENERAL HOSPITAL · PI SORENSEN, ALMA GREGORY · 2004 to 2004
$500k
Computeserver Structural &Functional Image AnalysisS10RR019307 · NCRR · MASSACHUSETTS GENERAL HOSPITAL · PI FISCHL, BRUCE · 2004 to 2004
$496k
NCRR NIH HHS P41 RR014075NCRR NIH HHS S10 RR019254NCRR NIH HHS S10 RR019307NCRR NIH HHS S10 RR021110NCRR NIH HHS S10 RR023043NCRR NIH HHS S10 RR023401NIA NIH HHS U01 AG024904NINDS NIH HHS P01 NS058793NINDS NIH HHS R01 NS042861NINDS NIH HHS R01 NS114562NINDS NIH HHS R56 NS042861NINR NIH HHS R01 NR010827
6 · The paper itself

Abstract

White matter signal abnormalities (WMSA), either hypo- or hyperintensities in MRI imaging, are considered a proxy of cerebrovascular pathology and contribute to, and modulate, the clinical presentation of Alzheimer's disease (AD), with cognitive dysfunction being apparent at lower levels of amyloid and/or tau pathology when lesions are present. To what extent the topography of cortical thinning associated with AD may be explained by WMSA remains unclear. Cortical thickness group difference maps and subgroup analyses show that the effect of WMSA on cortical thickness in cognitively normal participants has a higher overlap with the canonical pattern of AD, compared to AD participants. (Age and sex-matched group of 119 NC (AV45 PET negative, CDR = 0) versus 119 participants with AD (AV45 PET-positive, CDR > 0.5). The canonical patterns of cortical atrophy thought to be specific to Alzheimer's disease are strongly linked to cerebrovascular pathology supporting a reinterpretation of the classical models of AD suggesting that a part of the typical AD pattern is due to co-localized cortical loss before the onset of AD.

Indexed as

Alzheimer DiseaseCognitive DysfunctionWhite MatterAtrophyHumansMagnetic Resonance ImagingAgingAlzheimer's diseaseCortical thicknessVascular riskWhite matter hyperintensities

Identifiers

PMID35414420
PMCPMC9387174
OpenAlexW4223623913

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.