帕金森病和抑郁症患者脑组织Brodman9区域共同差异基因的生物信息学分析

doi:10.3969/j.issn.1006-6233.2022.12.008

Abstract
Figure/Table
References
Related Citation (15)

Download: PDF (2512 KB) HTML (1 KB)
Export: BibTeX | EndNote (RIS)

Abstract Objective: To provide common clues for the research on the mechanism between Parkinson Disease (PD) and major depression disease (MDD) by analyzing the common differential genes (DEGs), the common pathways and hub genes between PD and MDD in the Brodman9 (BA9) region of brain. Methods: GSE20168, GSE54567, GSE54568 and GSE54570 microarray data were downloaded from GEO database, and bioinformatics analysis packages such as limma, clusterProfiler and ggplot2 were called using R language to analyze PD and MDD co-expression with P<0. 05 and logFC absolute value ≥ 0. 3 as criteria. Differential genes were further analyzed by GO and KEGG enrichment for common pathways, and protein-protein interaction (PPI) networks and key genes were identified using String database and cytoscape software. Results: There were 34 common DEGs in the BA9 region of PD and MDD patients, and 21 were up-regulated: SLC35E1,ATP8B1,TSR1, ZNF721, RIOK3,FBXW12, ZNF160, POLR1B, CACNA1I, MZT2B, PGF, RP11-403P17. 4, RPL23AP32, DBT, PRR11, USP34, LRRFIP1, DSERG1, DIP2A, AEBP1 and DNAJB2, 13 genes were down-regulated, namely NPTX2, PCSK1, SST, PPP1CB, SEC22B, ENPP4, NME5, CAPZA2, GLRB, ITFG1, GLIPR1, TM6SF1 and DUSP6. The functional enrichment analysis of DEGs showed that there were 5 common GO_BP terms between PD and MDD, namely: GO:0007611 (learning or memory), GO:0050890 (cognition), GO:0007612 (learning), GO:0051384 (response to glucocorticoids), GO:0008306 (associative learning), suggesting that both PD and MDD have cognitive, learning, memory and glucocorticoid response pathway dysfunctions (P<0. 05). PPI network mapping and hub genes analysis indicated that NPTX2, PCSK1, DUSP6, SST, and PPP1CB genes may be the common hub genes among PD and MDD, and their levels were significantly decreased in both PD and MDD (P<0. 05). Conclusion: Cognitive pathway dysfunction and decreased expression of genes such as NPTX2 in BA9 region may be the common molecular pathology between PD and MDD.

Key words： Parkinson disease Major depression disease Bioinformatics Genes

	Service

	E-mail this article
	Add to my bookshelf
	Add to citation manager
	E-mail Alert
	RSS
	Articles by authors
	BAI Xue
	ZHAO Shumin
	CHEN Ranran
	et al

Cite this article:

BAI Xue,ZHAO Shumin,CHEN Ranran, et al. Common Differential Genes in the Brodman9 Region of Brain Tissues in Patients with Parkinson's Disease and Major Depression Disease: A Bioinformatics-Based Study[J]. HeBei Med, 2022, 28(12): 1985-1989.

URL:

http://www.hbyxzzs.cn/EN/10.3969/j.issn.1006-6233.2022.12.008 OR http://www.hbyxzzs.cn/EN/Y2022/V28/I12/1985

[1] 中华医学会神经病学分会帕金森病及运动障碍学组,中国医师协会神经内科医师分会帕金森病及运动障碍学组.中国帕金森病治疗指南(第四版)[J].中华神经科杂志,2020,53(12):973-986.
[2] 中华医学会精神医学分会抑郁障碍研究协作组.抑郁症认知症状评估与干预专家共识[J].中华精神科杂志,2020,53(5):8.
[3] Pizzagalli DA,Roberts AC.Prefrontal cortex and depression[J].Neuropsychopharmacology,2022,47(1):225-246.
[4] Pozdyshev DV,Zharikova AA,Medvedeva MV,et al.Differential analysis of A-to-I mRNA edited sites in parkinson's disease[J].Genes (Basel),2021,13(1):14.
[5] Randver R,Davel K,Toomsoo T.High-frequency repetitive transcranial magnetic stimulation to the left dorsolateral prefrontal cortex of patients with Parkinson's disease and treatment-resistant depression:a pilot study[J].Neurocase,2019,5(3-4):80-90.
[6] H,McClure MA,He L,Xiong L,et al.Antidepressant effects of repetitive transcranial magnetic stimulation over prefrontal cortex of parkinson's disease patients with depression:a meta-analysis[J].Front Psychiatry,2019,29(9):769.
[7] Okano M,Takahata K,Sugimoto J,et al.Selegiline recovers synaptic plasticity in the medial prefrontal cortex and improves corresponding depression-like behavior in a mouse model of parkinson's disease[J].Front Behav Neurosci,2019,2(13):176.
[8] Tang CZ,Zhang DF,Yang JT,et al.Overexpression of microRNA-301b accelerates hippocampal microglia activation and cognitive impairment in mice with depressive-like behavior through the NF-κB signaling pathway[J].Cell Death Dis,2019,10(4):316.
[9] Lang Y,Li Y,Yu H,et al.HOTAIR drives autophagy in midbrain dopaminergic neurons in the substantia nigra compacta in a mouse model of Parkinson's disease by elevating NPTX2 via miR-221-3p binding[J].Aging (Albany NY),2020,12(9):7660-7678.
[10] Boiten WA,van Steenoven I,Xiao MF,et al.Pathologically decreased CSF levels of synaptic marker NPTX2 in DLB are correlated with levels of alpha-synuclein and VGF[J].Cells,2020,10(1):38.
[11] Shakya M,Gahlot S,White A,et al.Mice lacking PC1/3 expression in POMC-expressing cells do not develop obesity[J].Endocrinology,2021,162(6):55.
[12] Iwasawa C,Kuzumaki N,Suda Y,et al.Reduced expression of somatostatin in GABAergic interneurons derived from induced pluripotent stem cells of patients with parkin mutations[J].Mol Brain,2019,12(1):5.
[13] Bertile F,Plumel M,Maes P,et al.Daytime restricted feeding affects day-night variations in mouse cerebellar proteome[J].Front Mol Neurosci,2021,12(14):613161.