Quantifying Personalized Shift-Work Molecular Portraits Underlying Alzheimer's Disease through Computational Biology

Research context and source limits

Limited evidence note. Only the source material identified below has been reviewed; this is not a complete Paper GEO V2 assessment.

Reported study components and clinical-substudy design; MR effect precision and molecular-score validation are unresolved.

Research question and study components

This computational study examines shift work, circadian-related molecular patterns and Alzheimer’s disease. Its Methods combine separate Mendelian-randomization analyses, public expression datasets and a proposed clock-deviation measure. These analytical components are identifiable, but their presence does not establish a causal effect of shift work or clinical validity of the proposed molecular score.

Source: Methods: Transcriptional data; Mendelian randomization analysis; clock-deviation-level analysis

Distinct clinical-substudy design

A separate retrospective clinical component reports 45 people with Alzheimer’s disease and 12 healthy participants recruited at one hospital. The Methods describe clinical assessment, hippocampal MRI in the Alzheimer’s group and sleep/chronotype questionnaires. This is distinct from the public expression samples and does not independently resolve the genetic analyses.

Source: Methods: Clinical data collection of the inhouse cohort

Unresolved interpretation

The reported OR confidence interval is inconsistent with the plotted beta-scale interval, and the main-text instrument count differs from the sensitivity supplement. GSE124870 is described as mouse day/night-shift data, whereas its official record specifies rat heart and shift-work/feeding conditions. These discrepancies prevent endorsement of the principal MR estimate and that validation claim.

Source: Article Abstract and MR Results; Figure 2B,D; Supplementary Table 4; Transcriptional data Methods and Figure 5E; GEO Series/Sample fields

Evidence limits

• No disputed effect size or causal conclusion is adopted.
• Clinical participants and expression-sample entries are not combined.

Provenance

• Article source — Official publisher or PMC full text reviewed locally. Methods: Transcriptional data; Mendelian randomization analysis; clock-deviation-level analysis
• Official dataset record — GEO Series metadata. Article Abstract and MR Results; Figure 2B,D; Supplementary Table 4; Transcriptional data Methods and Figure 5E; GEO Series/Sample fields

Source review: 2026-10-27.

Verify publication identity

These records identify the same original work; database inclusion is not evidence of scientific validity or clinical benefit.