ArticleProceedings of the National Academy of Sciences of the United States of America2016
A transcriptional signature of Alzheimer's disease is associated with a metastable subproteome at risk for aggregation.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 3 of them syntheses that pooled it.
What it found
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Who cites it
49 citing papers in PubMed, 3 syntheses or guidelines pooled it, 87 citations in OpenAlex.
- Integrative analysis of summary data from GWAS and eQTL studies implicates genes differentially expressed in Alzheimer's disease.BMC genomics · 2022Pooled it
- Systematic review and meta-analysis of human transcriptomics reveals neuroinflammation, deficient energy metabolism, and proteostasis failure across neurodegeneration.Neurobiology of disease · 2021Pooled it
- Meta-Analysis of Gene Expression Changes in the Blood of Patients with Mild Cognitive Impairment and Alzheimer's Disease Dementia.International journal of molecular sciences · 2019Pooled it
- Molecular signatures of regional vulnerability to tauopathy in excitatory cortical neurons.Acta neuropathologica · 2025Article
- Examining the vulnerability of adult neuron subtypes to tau-mediated toxicity in Drosophila.Translational psychiatry · 2025Article
- Nuclear respiratory factor-1 (NRF1) induction drives mitochondrial biogenesis and attenuates amyloid beta-induced mitochondrial dysfunction and neurotoxicity.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Article
- Astrocyte tau deposition in progressive supranuclear palsy is associated with dysregulation of MAPT transcription.Acta neuropathologica communications · 2024Article
- The ABC's of Alzheimer risk gene ABCA7.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Review
- Blood RNA transcripts show changes in inflammation and lipid metabolism in Alzheimer's disease and mitochondrial function in mild cognitive impairment.Journal of Alzheimer's disease reports · 2024Article
- Mechanisms and pathology of protein misfolding and aggregation.Nature reviews. Molecular cell biology · 2023Review
- Relationship BetweenJournal of Alzheimer's disease reports · 2023Article
- Characterization of gene expression patterns in mild cognitive impairment using a transcriptomics approach and neuroimaging endophenotypes.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2022Article
- Mapping the sequence specificity of heterotypic amyloid interactions enables the identification of aggregation modifiers.Nature communications · 2022Article
- An Outlook on the Complexity of Protein Morphogenesis in Health and Disease.Frontiers in molecular biosciences · 2022Review
- Differences in Immune-Related Genes Underlie Temporal and Regional Pathological Progression in 3xTg-AD Mice.Cells · 2022Article
- Cytosolic Quality Control of Mitochondrial Protein Precursors-The Early Stages of the Organelle Biogenesis.International journal of molecular sciences · 2021Review
- Deep post-GWAS analysis identifies potential risk genes and risk variants for Alzheimer's disease, providing new insights into its disease mechanisms.Scientific reports · 2021Article
- Article
- Current Trends in Neurodegeneration: Cross Talks between Oxidative Stress, Cell Death, and Inflammation.International journal of molecular sciences · 2021Review
- Mutations in the COPI coatomer subunit α-COP induce release of Aβ-42 and amyloid precursor protein intracellular domain and increase tau oligomerization and release.Neurobiology of aging · 2021Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
It is well-established that widespread transcriptional changes accompany the onset and progression of Alzheimer's disease. Because of the multifactorial nature of this neurodegenerative disorder and its complex relationship with aging, however, it remains unclear whether such changes are the result of nonspecific dysregulation and multisystem failure or instead are part of a coordinated response to cellular dysfunction. To address this problem in a systematic manner, we performed a meta-analysis of about 1,600 microarrays from human central nervous system tissues to identify transcriptional changes upon aging and as a result of Alzheimer's disease. Our strategy to discover a transcriptional signature of Alzheimer's disease revealed a set of down-regulated genes that encode proteins metastable to aggregation. Using this approach, we identified a small number of biochemical pathways, notably oxidative phosphorylation, enriched in proteins vulnerable to aggregation in control brains and encoded by genes down-regulated in Alzheimer's disease. These results suggest that the down-regulation of a metastable subproteome may help mitigate aberrant protein aggregation when protein homeostasis becomes compromised in Alzheimer's disease.
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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 OpenQuestion graph.