Evidence map›Paper›PMID 37528163›Full record

ArticleCommunications medicine2023

Cortical microstructural changes predict tau accumulation and episodic memory decline in older adults harboring amyloid.

Geoffroy Gagliardi, Elena Rodriguez-Vieitez, Victor Montal, Jorge Sepulcre, Ibai Diez, Cristina Lois, Bernard Hanseeuw, Aaron P Schultz, Michael J Properzi, Kathryn V Papp and 5 more

Open access · goldAbstract read
In one paragraph

Article in Communications medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

12 citing papers in PubMed, 11 citations in OpenAlex.

  1. Review
  2. Observational
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  11. Medial temporal lobe gray matter microstructure in preclinical Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    Article
  12. 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

15 authors at 4 institutions in 4 countries.

Geoffroy Gagliardi *Massachusetts General Hospital, Harvard Medical School, Boston, MA, 02114, USA.ORCID http://orcid.org/0000-0002-2608-8456
Elena Rodriguez-Vieitez *Massachusetts General Hospital, Harvard Medical School, Boston, MA, 02114, USA.ORCID http://orcid.org/0000-0002-6639-8141
Victor MontalSant Pau Memory Unit, Department of Neurology, Hospital de la Santa Creu i Sant Pau, Biomedical Research Institute Sant Pau, Universitat Autònoma de Barcelona, Barcelona, 08041, Spain.
Jorge SepulcreMassachusetts General Hospital, Harvard Medical School, Boston, MA, 02114, USA.
Ibai DiezMassachusetts General Hospital, Harvard Medical School, Boston, MA, 02114, USA.ORCID http://orcid.org/0000-0001-5769-0178
Cristina LoisMassachusetts General Hospital, Harvard Medical School, Boston, MA, 02114, USA.ORCID http://orcid.org/0000-0002-8766-2212
Bernard HanseeuwMassachusetts General Hospital, Harvard Medical School, Boston, MA, 02114, USA.
Aaron P SchultzMassachusetts General Hospital, Harvard Medical School, Boston, MA, 02114, USA.
Michael J ProperziMassachusetts General Hospital, Harvard Medical School, Boston, MA, 02114, USA.
Kathryn V PappMassachusetts General Hospital, Harvard Medical School, Boston, MA, 02114, USA.
Gad A MarshallMassachusetts General Hospital, Harvard Medical School, Boston, MA, 02114, USA.
Juan ForteaSant Pau Memory Unit, Department of Neurology, Hospital de la Santa Creu i Sant Pau, Biomedical Research Institute Sant Pau, Universitat Autònoma de Barcelona, Barcelona, 08041, Spain.
Keith A JohnsonMassachusetts General Hospital, Harvard Medical School, Boston, MA, 02114, USA.
Reisa A SperlingMassachusetts General Hospital, Harvard Medical School, Boston, MA, 02114, USA.ORCID http://orcid.org/0000-0003-1535-6133
Patrizia VanniniMassachusetts General Hospital, Harvard Medical School, Boston, MA, 02114, USA. patrizia@bwh.harvard.edu.ORCID http://orcid.org/0000-0002-9425-1059
Harvard University · USBrigham and Women's Hospital · USUniversitat Autònoma de Barcelona · ESCliniques Universitaires Saint-Luc · BE

Funding

Vascular factors, physical activity, and inflammation as modulators of neurodegenerative and cognitive trajectories (Project 2)P01AG036694 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI REISA A. SPERLING · 2010 to 2026
$50.2M
The Role of Inflammation and NGF Dysfunction in the Evolution of Alzheimer Disease Pathology in Down Syndrome-RevisionRF1AG056850 · NIA · UNIVERSITY OF CALIFORNIA-IRVINE · PI BUSCIGLIO, JORGE A, CUELLO, A CLAUDIO · 2018 to 2020
$5.9M
Decoding neural systems underlying anosognosia for memory loss in aging and Alzheimer's diseaseR01AG061083 · NIA · BRIGHAM AND WOMEN'S HOSPITAL · PI VANNINI, PATRIZIA · 2019 to 2023
$4.3M
Tau pathology in Down syndrome and Alzheimer'sRF1AG061566 · NIA · UNIVERSITY OF DENVER (COLORADO SEMINARY) · PI GRANHOLM-BENTLEY, ANN-CHARLOTTE ESTHER, MARGITTAI, MARTIN · 2019 to 2019
$3.4M
Genetic Profiles of the Spatiotemporal Causality of Tau and Amyloid in the Elderly BrainR01AG061445 · NIA · YALE UNIVERSITY · PI SEPULCRE, JORGE · 2019 to 2023
$1.9M
Sensory and Motor Streams in Preclinical and Clinical Stages of Alzheimer's DiseaseR01AG061811 · NIA · YALE UNIVERSITY · PI SEPULCRE, JORGE · 2019 to 2023
$1.7M
Novel diffusion-weighted MRI assessment of cortical microstructural changes and their relationship to amyloid, tau and cognition in aging and Alzheimer's disease.R21AG064348 · NIA · BRIGHAM AND WOMEN'S HOSPITAL · PI VANNINI, PATRIZIA · 2019 to 2020
$492k
Biological Correlates of Alzheimer in Down Syndrome.R21AG056974 · NIA · UNIVERSITY OF DENVER (COLORADO SEMINARY) · PI GRANHOLM-BENTLEY, ANN-CHARLOTTE ESTHER · 2017 to 2018
$414k
NIA NIH HHS P01 AG036694NIA NIH HHS R01 AG061083NIA NIH HHS R01 AG061445NIA NIH HHS R01 AG061811NIA NIH HHS R21 AG056974NIA NIH HHS R21 AG064348NIA NIH HHS RF1 AG056850NIA NIH HHS RF1 AG061566
6 · The paper itself

Abstract

introductionNon-invasive diffusion-weighted imaging (DWI) to assess brain microstructural changes via cortical mean diffusivity (cMD) has been shown to be cross-sectionally associated with tau in cognitively normal older adults, suggesting that it might be an early marker of neuronal injury. Here, we investigated how regional cortical microstructural changes measured by cMD are related to the longitudinal accumulation of regional tau as well as to episodic memory decline in cognitively normal individuals harboring amyloid pathology.

methods122 cognitively normal participants from the Harvard Aging Brain Study underwent DWI, T1w-MRI, amyloid and tau PET imaging, and Logical Memory Delayed Recall (LMDR) assessments. We assessed whether the interaction of baseline amyloid status and cMD (in entorhinal and inferior-temporal cortices) was associated with longitudinal regional tau accumulation and with longitudinal LMDR using separate linear mixed-effects models.

resultsWe find a significant interaction effect of the amyloid status and baseline cMD in predicting longitudinal tau in the entorhinal cortex (p = 0.044) but not the inferior temporal lobe, such that greater baseline cMD values predicts the accumulation of entorhinal tau in amyloid-positive participants. Moreover, we find a significant interaction effect of the amyloid status and baseline cMD in the entorhinal cortex (but not inferior temporal cMD) in predicting longitudinal LMDR (p < 0.001), such that baseline entorhinal cMD predicts the episodic memory decline in amyloid-positive participants.

conclusionsThe combination of amyloidosis and elevated cMD in the entorhinal cortex may help identify individuals at short-term risk of tau accumulation and Alzheimer's Disease-related episodic memory decline, suggesting utility in clinical trials.

Identifiers

PMID37528163
PMCPMC10394044
OpenAlexW4385457326

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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.