Evidence map›Paper›PMID 39513091›Full record

ReviewBrain communications2024

Cerebral hyperactivation across the Alzheimer's disease pathological cascade.

Nick Corriveau-Lecavalier, Jenna N Adams, Larissa Fischer, Eóin N Molloy, Anne Maass

Abstract readReview
In one paragraph

Review in Brain communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

35 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  16. Excitation-inhibition homeostasis in Alzheimer's disease: a selective multiscale review of mechanisms, sex differences, and therapeutic opportunities.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
    Review
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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

5 authors.

Nick Corriveau-LecavalierDepartment of Neurology, Mayo Clinic, Rochester, Minnesota 55902, USA.ORCID https://orcid.org/0000-0002-6561-9870
Jenna N AdamsDepartment of Neurobiology and Behavior, University of California, Irvine 92697, CA, USA.ORCID https://orcid.org/0000-0002-6702-3851
Larissa FischerGerman Center for Neurodegenerative Diseases, Magdeburg 39120, Germany.ORCID https://orcid.org/0009-0001-9936-2954
Eóin N MolloyGerman Center for Neurodegenerative Diseases, Magdeburg 39120, Germany.
Anne MaassGerman Center for Neurodegenerative Diseases, Magdeburg 39120, Germany.ORCID https://orcid.org/0000-0002-7889-795X

Funding

Effect of hippocampal tau pathology on CA1 function and memory processing in agingF32AG074621 · NIA · UNIVERSITY OF CALIFORNIA-IRVINE · PI ADAMS, JENNA NICOLE · 2021 to 2023
$202k
NIA NIH HHS F32 AG074621
6 · The paper itself

Abstract

Neuronal dysfunction in specific brain regions or across distributed brain networks is a known feature of Alzheimer's disease. An often reported finding in the early stage of the disease is the presence of increased functional MRI (fMRI) blood oxygenation level-dependent signal under task conditions relative to cognitively normal controls, a phenomenon known as 'hyperactivation'. However, research in the past decades yielded complex, sometimes conflicting results. The magnitude and topology of fMRI hyperactivation patterns have been found to vary across the preclinical and clinical spectrum of Alzheimer's disease, including concomitant 'hypoactivation' in some cases. These incongruences are likely due to a range of factors, including the disease stage at which the cohort is examined, the brain areas or networks studied and the fMRI paradigm utilized to evoke these functional abnormalities. Additionally, a perennial question pertains to the nature of hyperactivation in the context of Alzheimer's disease. Some propose it reflects compensatory mechanisms to sustain cognitive performance, while others suggest it is linked to the pathological disruption of a highly regulated homeostatic cycle that contributes to, or even drives, disease progression. Providing a coherent narrative for these empirical and conceptual discrepancies is paramount to develop disease models, understand the synergy between hyperactivation and the Alzheimer's disease pathological cascade and tailor effective interventions. We first provide a comprehensive overview of functional brain changes spanning the course from normal ageing to the clinical spectrum of Alzheimer's disease. We then highlight evidence supporting a close relationship between fMRI hyperactivation and

Indexed as

Alzheimer’s diseaseamyloidcerebral hyperactivationfMRItau

Identifiers

PMID39513091
PMCPMC11542485

What OpenQuestion holds

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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.