Evidence mapPaperPMID 37718796Full record

ArticleJournal of Alzheimer's disease : JAD2023

TOMM40 '523 Genotype Distinguishes Patterns of Cognitive Improvement for Executive Function in APOEɛ3 Homozygotes.

Amber Watts, Stephen Haneline, Kathleen A Welsh-Bohmer, Jingtao Wu, Robert Alexander, Russell H Swerdlow, Daniel K Burns, Ann M Saunders

Open access · hybridAbstract read
In one paragraph

Article in Journal of Alzheimer's disease : JAD, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.4field-weighted citation impact, top 36% 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

2 citing papers in PubMed, 2 citations in OpenAlex.

  1. Article
  2. 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 1 country.

Amber WattsUniversity of Kansas, Alzheimer's Disease Research Center, Fairway, KS, USA.
Stephen HanelineZinfandel Pharmaceuticals, Research Triangle Park, Chapel Hill, NC, USA.
Kathleen A Welsh-BohmerDuke University, Durham, NC, USA.
Jingtao WuTakeda Development Center Americas, Cambridge, MA, USA.
Robert AlexanderTakeda Development Center Americas, Cambridge, MA, USA.
Russell H SwerdlowUniversity of Kansas, Alzheimer's Disease Research Center, Fairway, KS, USA.
Daniel K BurnsZinfandel Pharmaceuticals, Research Triangle Park, Chapel Hill, NC, USA.
Ann M SaundersZinfandel Pharmaceuticals, Research Triangle Park, Chapel Hill, NC, USA.
Takeda (United States) · USUniversity of Kansas · USDuke University · US

Funding

Research Education ComponentP30AG072958 · DUKE UNIVERSITY · 2025 to 2025
$2.8M
NIA NIH HHS P30 AG072958
6 · The paper itself

Abstract

backgroundTOMM40 '523 has been associated with cognitive performance and risk for developing Alzheimer's disease independent of the effect of APOE genotype. Few studies have considered the longitudinal effect of this genotype on change in cognition over time.

objectiveOur objective was to evaluate the relationship between TOMM40 genotype status and change in cognitive performance in the TOMMORROW study, which was designed to prospectively evaluate an algorithm that includes TOMM40 '523 for genetic risk for conversion to mild cognitive impairment.

methodsWe used latent growth curve models to estimate the effect of TOMM40 allele carrier (short, very long) status on the intercept and slope of change in cognitive performance in four broad cognitive domains (attention, memory, executive function, and language) and a combined overall cognitive score over 30 months.

resultsTOMM40 very long allele carriers had significantly lower baseline performance for the combined overall cognitive function score (B = -0.088, p = 0.034) and for the executive function domain score (B = -0.143, p = 0.013). Slopes for TOMM40 very long carriers had significantly greater increases over time for the executive function domain score only. In sensitivity analyses, the results for executive function were observed in participants who remained clinically stable, but not in those who progressed clinically over the study duration.

conclusionsOur results add to the growing body of evidence that TOMM40, in the absence of APOEɛ4, may contribute to cognitive changes with aging and dementia and support the view that mitochondrial function is an important contributor to Alzheimer's disease risk.

Indexed as

Alzheimer DiseaseCognitive DysfunctionApolipoproteins ECognitionExecutive FunctionGenotypeHomozygoteHumansMitochondrial Precursor Protein Import Complex ProteinsApolipoproteins EMitochondrial Precursor Protein Import Complex ProteinsTOMM40 protein, humanAlzheimer’s diseaseAPOEcognitionexecutive functionlongitudinalTOMM40

Identifiers

PMID37718796
PMCPMC10578241
OpenAlexW4386768862

What Socratic holds

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LicenceCC BY
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Registered trials

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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 Socratic graph.