Differentially expressed genes related to age and the Alzheimer&rsquo;s disease

JI Kai-yuan MA Wen-li* ZHENG Wen-ling

doi:10.16098/j.issn.0529-1356.2015.02.004

Acta Anatomica Sinica ›› 2015, Vol. 46 ›› Issue (2) : 164-169. DOI: 10.16098/j.issn.0529-1356.2015.02.004

Differentially expressed genes related to age and the Alzheimer’s disease

JI Kai-yuan MA Wen-li* ZHENG Wen-ling

Author information +

History +

Abstract

Objective To study gene expression analysis of age related morbidity of the Alzheimer’s disease. Methods The Qlucore Omics Explore (QOE) bioinformatic software was used to analyze age and Alzheimer’s disease related gene expression data of GSE36980 and GSE53890 from Gene Expression Omnibus (GEO). Differentially expressed genes involved in Alzheimer’s disease and age were screened by two group comparison and linear regression in the case of strict compliance with statistical significance. Online tool software DAVID was used for Gene Ontology (GO) enrichment analysis. Results Twenty differentially expressed genes in Alzheimer’s disease were found to be down regulated with age. The result of GO enrichment analysis showed that the involved biological process of these genes was relevant to cellular protein catabolic process, cell cycle and neurological system process. It was also found that the genes were involved in cellular structural component, such as axon, synapse, plasma membrane, cytoskeleton and non-membrane-bounded organelle. The molecular functions involved were found to be adenyl ribonucleotide binding and metal ion binding. Conclusion Through data mining analysis, we find that in the Alzheimer’s disease, PDE2A and other 19 genes are down regulated with age. It indicates that these 20 genes are not only related with aging, but also involved in the mechanisms of Alzheimer’s diseases.

Key words

Alzheimer’s disease / Age / Gene expression / Bioinformatics / Human

Cite this article

EndNote

Ris (Procite)

Bibtex

Download Citations

JI Kai-yuan MA Wen-li* ZHENG Wen-ling. Differentially expressed genes related to age and the Alzheimer’s disease[J]. Acta Anatomica Sinica. 2015, 46(2): 164-169 https://doi.org/10.16098/j.issn.0529-1356.2015.02.004

References

［1］Falardeau M. Respect towards people with alzheimer’s disease［J］. Soins Gerontol, 2011(91): 10-12.
［2］Brookmeyer R, Johnson E, Ziegler-Graham K, et al. Forecasting the global burden of Alzheimer’s disease［J］. Alzheimers Dement, 2007, 3(3): 186-191.
［3］Bostrom AM, Van Soest D, Kolewaski B, et al. Nutrition status among residents living in a veterans’ longterm care facility in Western Canada: a pilot study［J］. J Am Med Dir Assoc, 2011, 12(3): 217-225.
［4］Thies W, Bleiler L. 2013 Alzheimer’s disease facts and figures［J］. Alzheimers Dement, 2013, 9(2): 208-245.
［5］Gilbert BJ. Republished: the role of amyloid beta in the pathogenesis of Alzheimer’s disease［J］. Postgrad Med J, 2014, 90(1060): 113-117.
［6］Hollingworth P, Harold D, Jones L, et al. Alzheimer’s disease genetics: current knowledge and future challenges［J］. Int J Geriatr Psychiatry, 2011, 26(8): 793-802.
［7］Anderton BH. Ageing of the brain［J］. Mech Ageing Dev, 2002, 123(7): 811-817.
［8］Imhof A, Kovari E, von Gunten A, et al. Morphological substrates of cognitive decline in nonagenarians and centenarians:a new paradigm［J］? J Neurol Sci, 2007, 257(1-2): 72-79.
［9］Mann DM, Tucker CM, Yates P O. The topographic distribution of senile plaques and neurofibrillary tangles in the brains of non-demented persons of different ages［J］. Neuropathol Appl Neurobiol, 1987, 13(2): 123-139.
［10］Jares P. DNA microarray applications in functional genomics［J］. Ultrastruct Pathol, 2006, 30(3): 209-219.
［11］Huang DW, Sherman BT, Lempicki RA. Systematic and integrative analysis of large gene lists using DAVID bioinformatics resources［J］. Nat Protoc, 2009, 4(1): 44-57.
［12］Arriagada PV, Marzloff K, Hyman BT. Distribution of Alzheimer-type pathologic changes in nondemented elderly individuals matches the pattern in Alzheimer’s disease［J］. Neurology, 1992, 42(9): 1681-1688.
［13］Bartzokis G. Alzheimer’s disease as homeostatic responses to age-related myelin breakdown［J］. Neurobiol Aging, 2011, 32(8): 1341-1371.
［14］Mann DM, Jones D. Deposition of amyloid (A4) protein within the brains of persons with dementing disorders other than Alzheimer’s disease and Down’s syndrome［J］. Neurosci Lett, 1990, 109(1-2): 68-75.
［15］Grudzien A, Shaw P, Weintraub S, et al. Locus coeruleus neurofibrillary degeneration in aging, mild cognitive impairmentand early Alzheimer’s disease［J］. Neurobiol Aging, 2007, 28(3): 327-335.
［16］Glenner GG, Wong CW. Alzheimer’s disease and Down’s syndrome: sharing of a unique cerebrovascular amyloid fibril protein［J］. Biochem Biophys Res Commun, 1984, 122(3): 1131-1135.
［17］GarciaSierra F, Hauw JJ, Duyckaerts C, et al. The extent of neurofibrillary pathology in perforant pathway neurons is the key determinant of dementia in the very old［J］. Acta Neuropathol, 2000, 100(1): 29-35.
［18］Knopman DS, Parisi JE, Salviati A, et al. Neuropathology of cognitively normal elderly［J］. J Neuropathol Exp Neurol, 2003, 62(11): 1087-1095.
［19］Armstrong RA. What causes Alzheimer’s disease［J］? Folia Neuropathol, 2013, 51(3): 169-188.
［20］Kovacs T. Therapy of Alzheimer disease［J］. Neuropsychopharmacol Hung, 2009, 11(1): 27-33.
［21］Chen Y, Qin LH, Chen XP, et al. Interfering effect and prohable mechanism of neregulin on experimental dementia model in rats ［J］. Acta Anatomica Sinica, 2010, 41(5): 666-669. (in Chinese)
陈燕，秦丽华，陈希平，等. 神经调节素对实验性痴呆大鼠的干预作用和可能机制［J］. 解剖学报, 2010,41(5): 666-669.