AlzBase: An Integrative Database for Gene Dysregulation in Alzheimer’s Disease
Abstract
Alzheimer's disease (AD) affects a significant portion of elderly people worldwide. Although the amyloid-β (Aβ) cascade hypothesis has been the prevailing theory for the molecular mechanism of AD in the past few decades, treatment strategies targeting the Aβ cascade have not demonstrated effectiveness as yet. Thus, elucidating the spatial and temporal evolution of the molecular pathways in AD remains to be a daunting task. To facilitate novel discoveries in this filed, here, we have integrated information from multiple sources for the better understanding of gene functions in AD pathogenesis. Several categories of information have been collected, including (1) gene dysregulation in AD and closely related processes/diseases such as aging and neurological disorders, (2) correlation of gene dysregulation with AD severity, (3) a wealth of annotations on the functional and regulatory information, and (4) network connections for gene-gene relationship. In addition, we have also provided a comprehensive summary for the top ranked genes in AlzBase. By evaluating the information curated in AlzBase, researchers can prioritize genes from their own research and generate novel hypothesis regarding the molecular mechanism of AD. To demonstrate the utility of AlzBase, we examined the genes from the genetic studies of AD. It revealed links between the upstream genetic variations and downstream endo-phenotype and suggested several genes with higher priority. This integrative database is freely available on the web at http://alz.big.ac.cn/alzBase .
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MITOL is supposed to be downregulated in patients with AD.
“It is supposed to be downregulated in patients with AD [131,132].”
From Role of Oxidative Damage in Alzheimer’s Disease and Neurodegeneration: From Pathogenic Mechanisms to Biomarker Discovery (2021) · cites this paper as [132]
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- Authors
- Bai, Z., Han, G., Xie, B., Wang, J., Song, F., Peng, X., & Lei, H.
- Affiliations
- Chinese Academy of Sciences (CN)
- Corresponding author
- Lei, Hongxing
- Venue
- Molecular Neurobiology
- Published
- 2014-11-29
- Volume
- 53
- Issue
- 1
- Pages
- 310-319
- ISSN
- 0893-7648 (ISSN-L)
- 1559-1182
- OpenAlex
- W2090485842
- Cited by
- 44
- References
- 68
- Citations by year
- 2026: 1 · 2025: 5 · 2024: 2 · 2023: 2 · 2022: 2 · 2021: 6 · 2020: 6 · 2019: 7 · 2018: 4 · 2017: 4 · 2016: 1 · 2015: 4
- FWCI
- 1.99
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Molecular Neurobiology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bioinformatics and Genomic Networks
- Keywords
- Alzheimer's disease, gene expression dysregulation, aging, disease severity, genetic variants, endophenotypes, molecular mechanisms, gene prioritization
- MeSH terms
- Aging, Alzheimer Disease, Brain, Gene Expression Regulation, Humans, Genetic Predisposition to Disease, Gene Expression Profiling, Databases, Genetic, Gene Regulatory Networks, Search Engine
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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