ArticleEMBO molecular medicine2023
Transfixed by transgenics: how pathology assumptions are slowing progress in Alzheimer's disease and related dementia research.
Article in EMBO molecular medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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.
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.
Who cites it
5 citing papers in PubMed.
- Sound-evoked auditory neurophysiological signals are a window into prodromal functional differences in a preclinical model of Alzheimer's disease.Scientific reports · 2026Article
- Treatment with BRICHOS domain helps to clarify issues with Alzheimer mouse models.EMBO molecular medicine · 2024Article
- Reply to Johansson 'Treatment with BRICHOS domain helps to clarify issues with Alzheimer mouse models'.EMBO molecular medicine · 2024Article
- Functional BRI2-TREM2 interactions in microglia: implications for Alzheimer's and related dementias.EMBO reports · 2024Article
- Transfixed by transgenics: how pathology assumptions are slowing progress in Alzheimer's disease and related dementia research.EMBO molecular medicine · 2023Article
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Abstract
Model organisms of human diseases are invaluable tools for unraveling pathogenic mechanisms, identifying potential targets for drug development, and evaluating the therapeutic efficacy of candidates in preclinical trials. The utility of model organisms hinges upon their ability to faithfully replicate the underlying pathogenic mechanisms of the human disease. For rodent models of Alzheimer's disease (AD) and AD-related dementias (ADRD), the limited translatability to human disease raises concerns about their overall utility. What factors contribute to this limitation? Is AD inherently too complex to be accurately modeled in nonhumans? Is the divergence between rodent brains and the human brain so pronounced that rodents are unsuitable as model organisms for AD? Or is it plausible that the commonly used rodent models don't capture the genuine pathogenic mechanisms underlying these diseases? This editorial discusses the challenges associated with transgenic models of AD and ADRD and offers some alternative approaches.
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Registered trials
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.