Evidence map›Paper›PMID 38102439›Full record

ArticleGeroScience2024

Early cerebral amyloid-β accumulation and hypermetabolism are associated with subtle cognitive deficits before accelerated cerebral atrophy.

Aftab Bakhtiari, Krisztina Benedek, Ian Law, Birgitte Fagerlund, Erik Lykke Mortensen, Merete Osler, Martin Lauritzen, Henrik B W Larsson, Mark B Vestergaard

Open access · hybridAbstract read
In one paragraph

Article in GeroScience, 2024. 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
1.9field-weighted citation impact, top 13% 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, 11 citations in OpenAlex.

  1. Sex differences in brain glucose metabolism and Alzheimer's disease risk and progression.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Review
  2. Early microglial response to amyloid plaques drives sleep loss in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Amyloid-Frontiers in aging neuroscience · 2026
    Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
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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

9 authors at 2 institutions in 1 country.

Aftab BakhtiariFunctional Imaging Unit, Department of Clinical Physiology and Nuclear Medicine, Rigshospitalet Glostrup, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark. aftab.bakhtiari@sund.ku.dk.ORCID 0000-0001-5651-480X
Krisztina BenedekDepartment of Neurology, Neurophysiology, Zealand University Hospital, Roskilde, Denmark.
Ian LawDepartment of Clinical Physiology and Nuclear Medicine, Rigshospitalet, , University of Copenhagen, Copenhagen, Denmark.
Birgitte FagerlundDepartment of Psychology, University of Copenhagen, Copenhagen, Denmark.
Erik Lykke MortensenDepartment of Public Health, University of Copenhagen, Copenhagen, Denmark.
Merete OslerDepartment of Public Health, University of Copenhagen, Copenhagen, Denmark.
Martin LauritzenDepartment of Clinical Neurophysiology, The Neuroscience Centre, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark.
Henrik B W LarssonFunctional Imaging Unit, Department of Clinical Physiology and Nuclear Medicine, Rigshospitalet Glostrup, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark.
Mark B VestergaardFunctional Imaging Unit, Department of Clinical Physiology and Nuclear Medicine, Rigshospitalet Glostrup, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark.
University of Copenhagen · DKZealand University Hospital · DK

Funding

Lundbeck Foundation R347-2020-217Velux Fonden VELUX26145
6 · The paper itself

Abstract

aimsAlzheimer's disease (AD) is characterized by the accumulation of amyloid beta (Aβ) in the brain. The deposition of Aβ is believed to initiate a detrimental cascade, including cerebral hypometabolism, accelerated brain atrophy, and cognitive problems-ultimately resulting in AD. However, the timing and causality of the cascade resulting in AD are not yet fully established. Therefore, we examined whether early Aβ accumulation affects cerebral glucose metabolism, atrophy rate, and age-related cognitive decline before the onset of neurodegenerative disease.

methodsParticipants from the Metropolit 1953 Danish Male Birth Cohort underwent brain positron emission tomography (PET) imaging using the radiotracers [

resultsHigher Aβ accumulation in AD-critical brain regions correlated with greater visual memory decline (p = 0.023). Aβ accumulation did not correlate with brain atrophy rates. Increased cerebral glucose metabolism in AD-susceptible regions correlated with worse verbal memory performance (p = 0.040).

conclusionsAβ accumulation in known AD-related areas was associated with subtle cognitive deficits. The association was observed before hypometabolism or accelerated brain atrophy, suggesting that Aβ accumulation is involved early in age-related cognitive dysfunction. The association between hypermetabolism and worse memory performance may be due to early compensatory mechanisms adapting for malfunctioning neurons by increasing metabolism.

Indexed as

Alzheimer DiseaseCognitive DysfunctionNeurodegenerative DiseasesAmyloid beta-PeptidesAtrophyCognitionGlucoseHumansMaleAmyloid beta-PeptidesGlucoseAgingAmyloidAtrophyCerebral glucose metabolismCognitionPET imaging

Identifiers

PMID38102439
PMCPMC10828321
OpenAlexW4389816730

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.