ArticleScientific reports2025
Alzheimer's disease may develop from changes in the immune system, cell cycle, and protein processing following alterations in ribosome function.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 6 papers, 1 of them a synthesis that pooled it.
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Rethinking Alzheimer's: novel miRNAs illuminate a disease beyond the brain.Molecular psychiatry · 2026Pooled it
- Engineering Nanoplatforms for Alzheimer's Disease Detection via Biomolecular Corona Proteomic and Lipidomic Profiling.Advanced healthcare materials · 2026Article
- An Exploratory Six-Probe Blood RNA Signature for Predicting 12-Month Cognitive Decline Along the Alzheimer's Disease Continuum: An Interpretable Machine Learning Study.Diagnostics (Basel, Switzerland) · 2026Article
- Intron Retention as a Homeostatic State Variable for Drug Response and Recovery: Lessons from Depression for Broader Applications.International journal of molecular sciences · 2026Review
- Unveiling ribosomal dysfunction and impaired signaling pathways in the cortical region of 5xFAD mice.Acta neuropathologica communications · 2026Article
- The interplay between recovery and immunity in infectious and non-communicable diseases.Frontiers in cellular and infection microbiology · 2026Review
Corrections and comments
- Erratum issued
Authors and funding
6 authors.
Funding
Abstract
The prevalence of Alzheimer's disease (AD) is increasing as society ages. The details of AD pathogenesis have not been fully elucidated, and a comprehensive gene expression analysis of the process leading up to the onset of AD would be helpful for understanding the mechanism. We performed an RNA sequencing analysis on a cohort of 1227 Japanese blood samples, representing 424 AD patients, 543 individuals with mild cognitive impairment (MCI), and 260 cognitively normal (CN) individuals. A total of 883 and 1169 statistically significant differentially expressed genes (DEGs) were identified between CN and MCI (CN-MCI) and between MCI and AD (MCI-AD), respectively. Pathway analyses using these DEGs, followed by protein-protein interaction network analysis, revealed key roles of ribosomal function in MCI progression, whereas immune responses, cell cycle, and protein processing in endoplasmic reticulum were involved in AD progression. Our findings indicate that the onset of AD might be associated with gene expression changes in the immune system, cell cycle, and protein processing following alterations in the expression of ribosomal protein genes during the MCI stage, although validation using brain tissue samples will be necessary in the future. Given the known effectiveness of delaying MCI progression in preventing AD, the genes related to ribosomal function might emerge as biomarkers for early diagnosis.
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