ArticlebioRxiv : the preprint server for biology2025
Insulin resistance alters cortical inhibitory neurons and microglia to exacerbate Alzheimer's knock-in mouse phenotypes.
Article in bioRxiv : the preprint server for biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
- Updated by
Authors and funding
5 authors.
Funding
Abstract
Metabolic dysfunction contributes to the risk and progression of Alzheimer's disease (AD) through insulin signaling, but the cellular mechanisms are not fully understood. In this study, we examined the effects of streptozotocin-induced insulin deficiency or a high-fat, high-sugar (HFHS) diet-induced insulin resistance on cognitive function in knock-in AD mouse models expressing human mutant APP and wild-type tau. Both metabolic perturbations caused hyperglycemia, but only the HFHS diet resulted in weight gain and greater learning and memory deficits. The HFHS diet exacerbation occurred without changes in amyloid-β or phospho-tau accumulation and with only subtle alterations in microglial morphology. The basis for functional deficits was explored with single-nucleus transcriptomic analysis. Prominent gene expression changes in glial cells and cerebral cortex Layer 2 inhibitory neurons correlated with the enhanced behavioral deficits. In HFHS-fed AD mice, we observed a shared
Identifiers
What Socratic holds
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 Socratic graph.