Evidence map›Paper›PMID 24658616›Full record

ArticleCerebral cortex (New York, N.Y. : 1991)2015

The Roots of Alzheimer's Disease: Are High-Expanding Cortical Areas Preferentially Targeted?†.

Anders M Fjell, Inge K Amlien, Markus H Sneve, Håkon Grydeland, Christian K Tamnes, Tristan A Chaplin, Marcello G P Rosa, Kristine B Walhovd

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cerebral cortex (New York, N.Y. : 1991), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

15 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
  2. Aging Brain from a Lifespan Perspective.Current topics in behavioral neurosciences · 2024
    Review
  3. Review
  4. Article
  5. Influence of Processing Pipeline on Cortical Thickness Measurement.Cerebral cortex (New York, N.Y. : 1991) · 2020
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
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  14. Article
  15. Review
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

8 authors at 3 institutions in 2 countries.

Anders M FjellResearch Group for Lifespan Changes in Brain and Cognition, Department of Psychology, University of Oslo, 0373 Norway Department of Physical Medicine and Rehabilitation, Unit of Neuropsychology, Oslo University Hospital, 0424 Norway.
Inge K AmlienResearch Group for Lifespan Changes in Brain and Cognition, Department of Psychology, University of Oslo, 0373 Norway.
Markus H SneveResearch Group for Lifespan Changes in Brain and Cognition, Department of Psychology, University of Oslo, 0373 Norway.
Håkon GrydelandResearch Group for Lifespan Changes in Brain and Cognition, Department of Psychology, University of Oslo, 0373 Norway.
Christian K TamnesResearch Group for Lifespan Changes in Brain and Cognition, Department of Psychology, University of Oslo, 0373 Norway.
Tristan A ChaplinDepartment of Physiology and Monash Vision Group, Monash University, Clayton, Victoria 3800, Australia ARC Centre of Excellence for Integrative Brain Function, Clayton, Victoria 3800, Australia.
Marcello G P RosaDepartment of Physiology and Monash Vision Group, Monash University, Clayton, Victoria 3800, Australia ARC Centre of Excellence for Integrative Brain Function, Clayton, Victoria 3800, Australia.
Kristine B WalhovdResearch Group for Lifespan Changes in Brain and Cognition, Department of Psychology, University of Oslo, 0373 Norway Department of Physical Medicine and Rehabilitation, Unit of Neuropsychology, Oslo University Hospital, 0424 Norway.
University of Oslo · NOARC Centre of Excellence for Integrative Brain Function · AUMonash University · AU

Funding

RECRUITMENT COREU19AG010483 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI FELDMAN, HOWARD · 2013 to 2020
$80.6M
NIA NIH HHS U19 AG010483
6 · The paper itself

Abstract

Alzheimer's disease (AD) is regarded a human-specific condition, and it has been suggested that brain regions highly expanded in humans compared with other primates are selectively targeted. We calculated shared and unique variance in the distribution of AD atrophy accounted for by cortical expansion between macaque and human, affiliation to the default mode network (DMN), ontogenetic development and normal aging. Cortical expansion was moderately related to atrophy, but a critical discrepancy was seen in the medial temporo-parietal episodic memory network. Identification of "hotspots" and "coldspots" of expansion across several primate species did not yield compelling evidence for the hypothesis that highly expanded regions are specifically targeted. Controlling for distribution of atrophy in aging substantially attenuated the expansion-AD relationship. A path model showed that all variables explained unique variance in AD atrophy but were generally mediated through aging. This supports a systems-vulnerability model, where critical networks are subject to various negative impacts, aging in particular, rather than being selectively targeted in AD. An alternative approach is suggested, focused on the interplay of the phylogenetically old and preserved medial temporal lobe areas with more highly expanded association cortices governed by different principles of plasticity and stability.

Indexed as

Brain MappingModels, NeurologicalAgedAged, 80 and overAgingAlzheimer DiseaseAnimalsAtrophyCerebral CortexFemaleHumansMacaca mulattaMaleMiddle AgedagingAlzheimer's diseasecerebral cortexdefault mode networkevolution

Identifiers

PMID24658616
PMCPMC6276920
OpenAlexW2114918703

What OpenQuestion holds

Textmetadata
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.