Abstract:
BACKGROUND:Alzheimer disease (AD) is a common neurodegenerative disorder with distinct pathological features, with aging considered the greatest risk factor. We explored how aging contributes to increased AD risk, and determined concurrent and coordinate changes (including genetic and phenotypic modifications) commonly exhibited in both normal aging and AD. METHODS:Using the Gene Expression Omnibus (GEO) database, we collected 1 healthy aging-related and 3 AD-related datasets of the hippocampal region. The normal aging dataset was divided into 3 age groups: young (20-40 years old), middle-aged (40-60 years old), and elderly (>60 years old). These datasets were used to analyze the differentially expressed genes (DEGs). The Gene Ontology (GO) terms, pathways, and function network analysis of these DEGs were analyzed. RESULTS:One thousand two hundred ninety-one DEGs were found to be shared in the natural aging groups and AD patients. Among the shared DEGs, ATP6V1E1, GNG3, NDUFV2, GOT1, USP14, and NAV2 have been previously found in both normal aging individuals and AD patients. Furthermore, using Java Enrichment of Pathways Extended to Topology (JEPETTO) analysis based on Kyoto Encyclopedia of Genes and Genomes (KEGG) database, we determined that changes in aging-related KEGG annotations may contribute to the aging-dependence of AD risk. Interestingly, NRXN3, the second most commonly deregulated gene identified in the present study, is known to carry a mutation in AD patients. According to functional network analysis, NRXN3 plays a critical role in synaptic functions involved in the cognitive decline associated with normal aging and AD. CONCLUSION:Our results indicate that the low expression of aging-related NRXN3 may increase AD risk, though the potential mechanism requires further clarification.
journal_name
Medicine (Baltimore)journal_title
Medicineauthors
Zheng JJ,Li WX,Liu JQ,Guo YC,Wang Q,Li GH,Dai SX,Huang JFdoi
10.1097/MD.0000000000011343subject
Has Abstractpub_date
2018-07-01 00:00:00pages
e11343issue
28eissn
0025-7974issn
1536-5964pii
00005792-201807130-00021journal_volume
97pub_type
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