ArticleFrontiers in aging neuroscience2021
Transcriptomic Changes Highly Similar to Alzheimer's Disease Are Observed in a Subpopulation of Individuals During Normal Brain Aging.
Article in Frontiers in aging neuroscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.
- Multi-omics and high-spatial-resolution omics: deciphering complexity in neurological disorders.GigaScience · 2025Pooled it
- Systems genetic dissection of brain gene expression reveals excitotoxic mechanisms of Alzheimer's disease.Molecular psychiatry · 2026Article
- A multi-omic atlas in the African turquoise killifish reveals increased glucocorticoid signaling as a hallmark of brain aging.bioRxiv : the preprint server for biology · 2026Article
- Integrated Multi-Tissue Transcriptomics Reveals Antagonistic Pleiotropy in Aging and Alzheimer's Disease.Computational and structural biotechnology journal · 2026Article
- Editorial: The stem cell niche in brain aging and neurodegenerative disorders.Frontiers in aging neuroscience · 2026Article
- Distinct migration patterns of adult neural stem cells derived from hippocampal and ventricular niches.Frontiers in aging neuroscience · 2026Article
- Conserved Blood Transcriptome Patterns Highlight microRNA and Hub Gene Drivers of Neurodegeneration.Genes · 2025Article
- Disruption of the cerebrospinal fluid-plasma protein balance in cognitive impairment and aging.Nature medicine · 2025Article
- Supervised multiple kernel learning approaches for multi-omics data integration.BioData mining · 2024Article
- Article
- Editorial: Bioinformatics analysis of single cell sequencing and multi-omics in the aging and age-associated diseases.Frontiers in aging neuroscience · 2024Article
- Neuronal activation of GCell reports · 2023Article
- Age-Related Modifications of Electroencephalogram Coherence in Mice Models of Alzheimer's Disease and Amyotrophic Lateral Sclerosis.Biomedicines · 2023Article
- SAPFIR: A webserver for the identification of alternative protein features.BMC bioinformatics · 2022Article
- Sphingolipid Metabolism as a New Predictive Target Correlated with Aging and AD: A Transcriptomic Analysis.Medicina (Kaunas, Lithuania) · 2022Article
- Microglia in Alzheimer's Disease: a Key Player in the Transition Between Homeostasis and Pathogenesis.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022Review
- Multi-omics analysis reveals neuroinflammation, activated glial signaling, and dysregulated synaptic signaling and metabolism in the hippocampus of aged mice.Frontiers in aging neuroscience · 2022Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Aging is a major risk factor for late-onset Alzheimer's disease (LOAD). How aging contributes to the development of LOAD remains elusive. In this study, we examined multiple large-scale transcriptomic datasets from both normal aging and LOAD brains to understand the molecular interconnection between aging and LOAD. We found that shared gene expression changes between aging and LOAD are mostly seen in the hippocampal and several cortical regions. In the hippocampus, the expression of phosphoprotein, alternative splicing and cytoskeleton genes are commonly changed in both aging and AD, while synapse, ion transport, and synaptic vesicle genes are commonly down-regulated. Aging-specific changes are associated with acetylation and methylation, while LOAD-specific changes are more related to glycoprotein (both up- and down-regulations), inflammatory response (up-regulation), myelin sheath and lipoprotein (down-regulation). We also found that normal aging brain transcriptomes from relatively young donors (45-70 years old) clustered into several subgroups and some subgroups showed gene expression changes highly similar to those seen in LOAD brains. Using brain transcriptomic datasets from another cohort of older individuals (>70 years), we found that samples from cognitively normal older individuals clustered with the "healthy aging" subgroup while AD samples mainly clustered with the "AD similar" subgroups. This may imply that individuals in the healthy aging subgroup will likely remain cognitively normal when they become older and vice versa. In summary, our results suggest that on the transcriptome level, aging and LOAD have strong interconnections in some brain regions in a subpopulation of cognitively normal aging individuals. This supports the theory that the initiation of LOAD occurs decades earlier than the manifestation of clinical phenotype and it may be essential to closely study the "normal brain aging" to identify the very early molecular events that may lead to LOAD development.
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Registered trials
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