Evidence map›Paper›PMID 26441321›Full record

ArticleHuman brain mapping2016

Spatial patterns of atrophy, hypometabolism, and amyloid deposition in Alzheimer's disease correspond to dissociable functional brain networks.

Michel J Grothe, Stefan J Teipel, Alzheimer's Disease Neuroimaging Initiative

Abstract read
In one paragraph

Article in Human brain mapping, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
90citing papers in PubMed, 3 pooled it
6.8field-weighted citation impact, top 2% 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

90 citing papers in PubMed, 3 syntheses or guidelines pooled it, 154 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. Article
  6. Mapping individual molecular connectomes in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
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  16. Sex-specific topological structure associated with dementia via latent space estimation.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
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30 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

Michel J GrotheGerman Center for Neurodegenerative Diseases (DZNE), Gehlsheimer Str. 20, Rostock, 18147, Germany.
Stefan J TeipelGerman Center for Neurodegenerative Diseases (DZNE), Gehlsheimer Str. 20, Rostock, 18147, Germany.
Alzheimer's Disease Neuroimaging Initiative
German Center for Neurodegenerative Diseases · DE

Funding

Alzheimer's Disease Neuroimaging Initiative - SupplementU01AG024904 · NIA · NORTHERN CALIFORNIA INSTITUTE RES &EDUC · PI WEINER, MICHAEL W · 2004 to 2015
$121.0M
NIA NIH HHS U01 AG024904
6 · The paper itself

Abstract

Recent neuroimaging studies of Alzheimer's disease (AD) have emphasized topographical similarities between AD-related brain changes and a prominent cortical association network called the default-mode network (DMN). However, the specificity of distinct imaging abnormalities for the DMN compared to other intrinsic connectivity networks (ICNs) of the limbic and heteromodal association cortex has not yet been examined systematically. We assessed regional amyloid load using AV45-PET, neuronal metabolism using FDG-PET, and gray matter volume using structural MRI in 473 participants from the Alzheimer's Disease Neuroimaging Initiative, including preclinical, predementia, and clinically manifest AD stages. Complementary region-of-interest and voxel-based analyses were used to assess disease stage- and modality-specific changes within seven principle ICNs of the human brain as defined by a standardized functional connectivity atlas. Amyloid deposition in AD dementia showed a preference for the DMN, but high effect sizes were also observed for other neocortical ICNs, most notably the frontoparietal-control network. Atrophic changes were most specific for an anterior limbic network, followed by the DMN, whereas other neocortical networks were relatively spared. Hypometabolism appeared to be a mixture of both amyloid- and atrophy-related profiles. Similar patterns of modality-dependent network specificity were also observed in the predementia and, for amyloid deposition, in the preclinical stage. These quantitative data confirm a high vulnerability of the DMN for multimodal imaging abnormalities in AD. However, rather than being selective for the DMN, imaging abnormalities more generally affect higher order cognitive networks and, importantly, the vulnerability profiles of these networks markedly differ for distinct aspects of AD pathology.

Indexed as

Alzheimer DiseaseAgedAged, 80 and overAmyloidAtrophyBrainFemaleFluorodeoxyglucose F18HumansImage Processing, Computer-AssistedMagnetic Resonance ImagingMaleMental Status ScheduleMetabolic DiseasesMiddle AgedModels, NeurologicalAmyloidFluorodeoxyglucose F18RadiopharmaceuticalsAV45-PETdefault mode networkFDG-PETintrinsic connectivity networksmild cognitive impairmentpreclinicalpredementiaresting-state functional MRIvoxel-based

Identifiers

PMID26441321
PMCPMC4715545
OpenAlexW1913607034

What OpenQuestion holds

Textmetadata
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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.