Evidence mapPaperPMID 41393111Full record

ArticleFrontiers in aging neuroscience2025

Are current etiological theories of Alzheimer's disease falsifiable? An epistemological assessment.

Tommaso Costa, Donato Liloia

Abstract read
In one paragraph

Article in Frontiers in aging neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
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

1 citing paper in PubMed.

  1. Genomic and proteomic conversion of brain ischemia to Alzheimer's disease.Frontiers in cell and developmental biology · 2026
    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

2 authors.

Tommaso CostaFunctional Neuroimaging and Complex Neural Systems (FOCUS) Laboratory, Department of Psychology, University of Turin, Turin, Italy.
Donato LiloiaFunctional Neuroimaging and Complex Neural Systems (FOCUS) Laboratory, Department of Psychology, University of Turin, Turin, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) research is plagued by a proliferation of competing etiological theories, often coexisting without undergoing systematic critical comparison. This article examines the epistemological limitations of the traditional falsifiability criterion, formulated by Karl Popper, and demonstrates how this principle fails to function effectively in the context of AD research. Biological complexity, the absence of unequivocal biomarkers, institutional resistance to paradigm shifts, and academic incentives to preserve dominant hypotheses all contribute to the erosion of falsifiability as an operational standard. In response, we propose an alternative framework based on Bayesian inference, understood as eliminative induction-a process in which scientific theories are modeled as probabilistic hypotheses with gradable plausibility, continuously updated considering new evidence. Within this framework, models are not regarded as literally "true," but as pragmatic tools whose predictive performance determines their scientific value. We advocate for a more comparative, predictive, and transparent scientific practice, wherein progress does not hinge on identifying a unique cause or on proving (or disproving) a hypothesis, but rather on enhancing our ability to rationally distinguish among competing models using quantitative criteria.

Indexed as

Bayesian inferenceeliminative inductionepistemology of sciencefalsifiabilitypredictive modelingscientific modelsscientific rationalitytheory comparison

Identifiers

PMID41393111
PMCPMC12698584

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.