ArticleMolecular neurobiology2025
Screening and In Vivo Validation of Key Genes Involved in Myelin Damage in Alzheimer's Disease.
Article in Molecular neurobiology, 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
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
Myelin sheath damage exacerbates cognitive deterioration in Alzheimer's disease (AD). This study identified 11 key genes related to myelin sheath damage between AD and control samples based on the GSE118553 dataset, and their expression was verified in the AD mouse model. Furthermore, the damage to myelin and synapses as well as the expression of the insulin receptor substrate-1 (IRS-1) and phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/glycogen synthase kinase-3β (GSK3β) signaling pathway proteins were observed by transmission electron microscopy and molecular biology techniques. The results confirmed that the expression of 8 out of 11 key genes was downregulated in mice with AD, which showed amyloid β-protein (Aβ) deposition, tau hyperphosphorylation, myelin and synaptic damage, and an abnormal expression of IRS-1/PI3K/Akt/GSK3β signaling and glucose transporter1/3 (GLUT1/3). This study provides a basis for the in-depth exploration of the gene regulatory mechanisms of myelin sheath injury in AD.
Indexed as
Identifiers
41317273What 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.