SynthesisScientific reports2022
Alzheimer's disease large-scale gene expression portrait identifies exercise as the top theoretical treatment.
Synthesis in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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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.
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Who cites it
40 citing papers in PubMed, 53 citations in OpenAlex.
- Isoform Remodeling and Promoter Switching Identify Altered Transcriptional Regulation in Alzheimer's Disease Frontal Cortex.Research square · 2026Article
- A Cross-Region Meta-Analysis and Machine Learning Identifies a 37-Gene Signature Associated with Alzheimer's Disease.Biomedicines · 2026Article
- Exercise and fluoxetine in Alzheimer's disease: Molecular mechanisms of synergistic and antagonistic effects (Review).International journal of molecular medicine · 2026Review
- Article
- Identification of Alzheimer's disease subtypes and biomarkers from human multi-omics data using subspace merging algorithm.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Aerobic exercise significantly altersJournal of Alzheimer's disease : JAD · 2026Article
- Unknotting the Role of circRNAs and IGF2BP3 in Alzheimer's Disease.Cellular and molecular neurobiology · 2026Review
- Cognitive impairment caused by compromised hepatic ketogenesis is prevented by endurance exercise.The Journal of physiology · 2026Article
- Regulon Reconstruction Uncovers Novel Deregulated Factors in Alzheimer's Disease.Molecular neurobiology · 2026Article
- Entorhinal Cholecystokinin in Alzheimer's Disease: Its Earliest Vulnerability and Rescue Effects Across Different Disease Stages in a Mouse Model.Cellular and molecular neurobiology · 2026Article
- Article
- Utilisation of Machine Learning Approaches Improves RNA-Seq Transcriptome Analyses in Alzheimer's Disease Brain.Journal of molecular neuroscience : MN · 2026Article
- Identification ofFrontiers in aging neuroscience · 2026Article
- Spatially resolved transcriptomics reveals a unique disease signature and potential biomarkers for chronic traumatic encephalopathy.Journal of neuropathology and experimental neurology · 2025Article
- Transcriptomic profiling of the middle temporal gyrus reveals differential glial/neuronal dysregulation across Alzheimer's disease and aging.bioRxiv : the preprint server for biology · 2025Article
- Transcriptomic and protein analysis of human cortex reveals genes and pathways linked to NPTX2 disruption in Alzheimer's disease.bioRxiv : the preprint server for biology · 2025Article
- Alzheimer's disease signatures in the brain transcriptome of Estuarine Dolphins.Communications biology · 2025Article
- An Indicator Cell Assay-based Multivariate Blood Test for Early Detection of Alzheimer's Disease.medRxiv : the preprint server for health sciences · 2025Article
- Aerobic exercise-induced changes in fluid biomarkers in Parkinson's disease.NPJ Parkinson's disease · 2025Review
- Identification of GABBR2 as a diagnostic marker and its association with Aβ in Alzheimer's disease.Biochemistry and biophysics reports · 2025Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Alzheimer's disease (AD) is a complex neurodegenerative disorder that affects multiple brain regions and is difficult to treat. In this study we used 22 AD large-scale gene expression datasets to identify a consistent underlying portrait of AD gene expression across multiple brain regions. Then we used the portrait as a platform for identifying treatments that could reverse AD dysregulated expression patterns. Enrichment of dysregulated AD genes included multiple processes, ranging from cell adhesion to CNS development. The three most dysregulated genes in the AD portrait were the inositol trisphosphate kinase, ITPKB (upregulated), the astrocyte specific intermediate filament protein, GFAP (upregulated), and the rho GTPase, RHOQ (upregulated). 41 of the top AD dysregulated genes were also identified in a recent human AD GWAS study, including PNOC, C4B, and BCL11A. 42 transcription factors were identified that were both dysregulated in AD and that in turn affect expression of other AD dysregulated genes. Male and female AD portraits were highly congruent. Out of over 250 treatments, three datasets for exercise or activity were identified as the top three theoretical treatments for AD via reversal of large-scale gene expression patterns. Exercise reversed expression patterns of hundreds of AD genes across multiple categories, including cytoskeleton, blood vessel development, mitochondrion, and interferon-stimulated related genes. Exercise also ranked as the best treatment across a majority of individual region-specific AD datasets and meta-analysis AD datasets. Fluoxetine also scored well and a theoretical combination of fluoxetine and exercise reversed 549 AD genes. Other positive treatments included curcumin. Comparisons of the AD portrait to a recent depression portrait revealed a high congruence of downregulated genes in both. Together, the AD portrait provides a new platform for understanding AD and identifying potential treatments for AD.
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