Advances in research on resting brain network functional magnetic resonance imaging for PD with cognitive impairmente

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WANG Qing XIA Jianguo TIAN Weizhong

Cite this article as: Wang Q, Xia JG, Tian WZ. Advances in research on resting brain network functional magnetic resonance imaging for PD with cognitive impairment. Chin J Magn Reson Imaging, 2020, 11(11): 1044-1047. DOI:10.12015/issn.1674-8034.2020.11.020.

Abstract

[Abstract] Resting state functional magnetic resonance imaging (RS-fMRI) has been widely used to analyze the pathophysiology of neurodegenerative diseases such as Parkinson's disease (PD). Parkinson's patients with cognitive impairment experience changes in their functional network connections that can lead to cognitive decline.In this review, we attempt to summarize recent RS-fMRI studies and discuss the limitations and potential significance of functional connectivity features in early Parkinson's disease to track and predict future PD progression. Understanding the neurologic factors and potential triggers of clinical progression and complications is important to guide new clinical trials and develop prevention strategies.

[Keywords] functional magnetic resonance imaging；imaging；biomarkers；Parkinson's disease；cognitive dysfunction；resting state network

Contributor Information

WANG Qing Graduate School of Dalian Medical University, Dalian 116044, China

XIA Jianguo^* Department of Radiology, Taizhou People's Hospital of Jiangsu Province, Taizhou 225300, China

TIAN Weizhong Department of Radiology, Taizhou People's Hospital of Jiangsu Province, Taizhou 225300, China

*Correspondence to: Xia JG, E-mail: shjxct@163.com

Conflicts of interest None.

Publication Information

ACKNOWLEDGMENTS This article is supported by the Scientific Research Project of Jiangsu Provincial Health Commission No. H2018093 Jiangsu Province Phase 5 "Project 333" Scientific Research Project No. BRA2017175

Received 2020-03-09

Accepted 2020-09-18

DOI: 10.12015/issn.1674-8034.2020.11.020

Text

References

[1]

Al-Radaideh AM, Rababah EM. The role of magnetic resonance imaging in the diagnosis of Parkinson's disease: a review. Clin Imag, 2016, 40(5): 987-996. DOI: 10.1016/j.clinimag.2016.05.006

[2]

Postuma RB, Berg D, Stern M, et al. MDS clinical diagnostic criteria for Parkinson’s disease. Mov Disord, 2015, 30(12): 1591-1601.

[3]

Yarnall AJ, Breen DP, Duncan GW, et al. Characterizing mild cognitive impairment in incident Parkinson disease: the ICICLE-PD study. Neurology, 2014, 82(4): 308-316.

[4]

Fengler S, Liepelt-Scarfone I, Brockmann K, et al. Cognitive changes in prodromal Parkinson's disease: a review. Mov Disord, 2017, 32(12): 1655-1666. DOI: 10.1002/mds.27135

[5]

Svenningsson P, Westman E, Ballard C, et al. Cognitive impairment in patients with Parkinson's disease: diagnosis, biomarkers, and treatment. Lancet Neurology, 2012, 11(8): 697-707.

[6]

袁悦铭,张力,张治国．基于静息态功能磁共振成像的动态功能连接分析及临床应用研究进展．磁共振成像, 2018, 9(8): 579-588. DOI: 10.12015/issn.1674-8034.2018.08.005

[7]

秦丽，宋远见，杨荣礼，等. HDAC6和p38信号分子在神经炎症中的研究现状．国际老年医学杂志, 2018, 39(1):40-44. DOI: 10.3969/j.issn.1674-7593.2018.01.011

[8]

Delgado-Alvarado M, Gago B, Navalpotro-Gomez I, et al. Biomarkers for dementia and mild cognitive impairment in Parkinson's disease. Mov Disord, 2016, 31(6):861-881. DOI: 10.1002/mds.26662

[9]

Adler CH, Beach TG. Neuropathological basis of nonmotor manifestations of Parkinson' s disease. Mov Disord, 2016, 31(8): 1114-1119. DOI: 10.1002/mds.26605

[10]

Surmeier DJ, Obeso JA, Halliday GM. Selective neuronal vulnerability in Parkinson disease. nature reviews. Neuroscience, 2017, 18(2): 101-113. DOI: 10.1038/nrn.2016.178

[11]

Bmedsci MC, Bsc HC, Halliday GM. Neuropathology of α-synuclein propagation and braak hypothesis. Mov Disord, 2016, 31(2): 152-160. DOI: 10.1002/mds.26421

[12]

Skogseth RE, Bronnick K, Pereira JB, et al. Associations between cerebrospinal fluid biomarkers and cognition in early untreated Parkinson's disease. J Parkinson's Dis, 2015, 5(4): 783-792. DOI: 10.3233/JPD-150682

[13]

Halliday GM, Leverenz JB, Schneider JS, et al. The neurobiological basis of cognitive impairment in Parkinson's disease. Mov Disord, 2014, 29(5): 634-650. DOI: 10.1002/mds.25857

[14]

Petrou M, Bohnen NI, Müller ML, et al. Aβ-amyloid deposition in patients with Parkinson disease at risk for development of dementia. Neurology, 2012, 79(11):1161-1167. DOI: 10.1212/WNL.0b013e3182698d4a

[15]

Compta Y, Parkkinen L, O'Sullivan SS, et al. Lewy- and Alzheimer-type pathologies in Parkinson's disease dementia: which is more important? Brain, 2011, 134(Pt 5): 1493-1505. DOI: 10.1093/brain/awr031

[16]

Kehagia AA, Barker RA, Robbins TW. Cognitive impairment in Parkinson's disease: the dual syndrome hypothesis. Neurodegener Dis, 2013, 11(2):79-92. DOI: 10.1159/000341998

[17]

Morley JF, Xie SX, Hurtig HI, et al. Genetic influences on cognitive decline in Parkinson's disease. Mov Disord, 2012, 27(4): 512-518. DOI: 10.1002/mds.24946

[18]

Brockmann K, Srulijes K, Pflederer S, et al. GBA-associated Parkinson's disease: reduced survival and more rapid progression in a prospective longitudinal study. Mov Disord, 2015, 30(3): 407-411. DOI: 10.1002/mds.26071

[19]

Winder-Rhodes SE, Hampshire A, Rowe JB, et al. Association between MAPT haplotype and memory function in patients with Parkinson's disease and healthy aging individuals. Neurobiol Aging, 2015, 36(3): 1519-1528. DOI: 10.1016/j.neurobiolaging.2014.12.006

[20]

Shah D, Blockx I, Guns PJ, et al. Acute modulation of the cholinergic system in the mouse brain detected by pharmacological resting-state functional MRI. Neuroimage, 2015, 109:151-159. DOI: 10.1016/j.neuroimage.2015.01.009

[21]

Zheng H, Onoda K, Wada Y, et al. Serotonin-1A receptor C-1019G polymorphism affects brain functional networks. Sci Rep, 2017, 7(1):12536. DOI: 10.1038/s41598-017-12913-3

[22]

Klaassens BL, van Gorsel HC, Khalili-Mahani N, et al. Single-dose serotonergic stimulation shows widespread effects on functional brain connectivity. Neuroimage, 2015, 122: 440-450. DOI: 10.1016/j.neuroimage.2015.08.012

[23]

Lin WC, Chen HL, Hsu TW, et al. Correlation between dopamine transporter degradation and striatocortical network alteration in Parkinson's diseasee. Front Neurol, 2017, 8: 323. DOI: 10.3389/fneur.2017.00323

[24]

Campbell MC, Koller JM, Snyder AZ, et al. CSF proteins and resting-state functional connectivity in Parkinson disease. Neurology, 2015, 84(24): 2413-2421. DOI: 10.1212/WNL.0000000000001681

[25]

陈怡，余成新．基于静息态功能磁共振成像的静态及动态功能连接分析方法研究进展．磁共振成像, 2019, 10(8): 637-640. DOI: 10.12015/issn.1674-8034.2019.08.017

[26]

Smitha KA, Akhil RK, Arun KM, et al. Resting state fMRI: a review on methods in resting state connectivity analysis and resting state networks. Neuroradiol J, 2017, 30(4): 305-317.

[27]

Filippi M, Elisabetta S, Piramide N, et al. Functional MRI in Idiopathic Parkinson's Disease.Int Rev Neurobiol, 2018, 141:439-467. DOI: 10.1177/1971400917697342

[28]

Putcha D, Ross RS, Cronin-Golomb A, et al. Altered intrinsic functional coupling between core neurocognitive networks in Parkinson's disease. Neuroimage, 2015, 7: 449-455. DOI: 10.1016/j.nicl.2015.01.012

[29]

Putcha D, Ross RS, Cronin-Golomb A, et al. Salience and default mode network coupling predicts cognition in aging and Parkinson's disease. J Int Neuropsychol Soc, 2016, 22(2):205-215. DOI: 10.1017/S1355617715000892

[30]

Sang L, Zhang J, Wang L, et al. Alteration of brain functional networks in early-stage Parkinson's disease: a resting-state fMRI study. PLoS One, 2015, 10(10): e0141815. DOI: 10.1371/journal.pone.0141815

[31]

Berman BD, Smucny J, Wylie KP, et al. Levodopa modulates small-world architecture of functional brain networks in Parkinson's disease. Mov Disord, 2016, 31(11): 1676-1684. DOI: 10.1002/mds.26713

[32]

Lopes R, Delmaire C, Defebvre L, et al. Cognitive phenotypes in Parkinson's disease differ in terms of Brain-Network Organization and Connectivity. Hum Brain Mapp, 2017, 38(3): 1604-1621. DOI: 10.1002/hbm.23474

[33]

Fang GP, Chen HM, Cao ZT, et al. Impaired brain network architecture in newly diagnosed Parkinson’s disease based on graph theoretical analysis. Neurosci Lett, 2017, 657: 151-158. DOI: 10.1016/j.neulet.2017.08.002

[34]

Suo X, Lei D, Li N, et al. Functional brain connectome and its relation to hoehn and yahr stage in Parkinson disease. Radiology, 2017, 285(3): 904-913. DOI: 10.1148/radiol.2017162929

[35]

Ma LY, Chen XD, He Y, et al. Disrupted brain network hubs in subtype-specific Parkinson's disease. Eur Neurol, 2017, 78(3-4): 200-209. DOI: 10.1159/000477902

[36]

de Schipper LJ, Hafkemeijer A, van der Grond J, et al. Altered whole-brain and network-based functional connectivity in Parkinson’s disease. Front Neurol, 2018, 9: 419. DOI: 10.3389/fneur.2018.00419

[37]

Hou Y, Wei Q, Ou R, et al. Impaired topographic organization in cognitively unimpaired drug-naïve patients with rigidity-dominant Parkinson's disease. Parkinsonism Relat D, 2018, 56: 52-57. DOI: 10.1016/j.parkreldis.2018.06.021

[38]

Badea L, Onu M, Wu T, et al. Exploring the reproducibility of functional connectivity alterations in Parkinson's disease. PloS one, 2017, 12(11): e0188196. DOI: 10.1371/journal.pone.0188196

[39]

O'Connor EE, Zeffiro TA. Why is clinical fMRI in a resting state? Front Neurol, 2019, 10:420. DOI: 10.3389/fneur.2019.00420

[40]

Gordon EM, Laumann TO, Adeyemo B, et al. Individual-specific features of brain systems identified with resting state functional correlations. Neuroimage, 2017, 146: 918-939. DOI: 10.1016/j.neuroimage.2016.08.032

[41]

Madhyastha TM, Askren MK, Zhang J, Let al. Group comparison of spatiotemporal dynamics of intrinsic networks in Parkinson's disease. Brain, 2015, 138(Pt 9): 2672-2686. DOI: 10.1093/brain/awv189

[42]

Gorges M, Müller HP, Lulé D, et al. To rise and to fall: functional connectivity in cognitively normal and cognitively impaired patients with Parkinson's disease. Neurobiol Aging, 2015, 36(4): 1727-1735. DOI: 10.1016/j.neurobiolaging.2014.12.026

[43]

Lebedev AV, Westman E, Simmons A, et al. Large-scale resting state network correlates of cognitive impairment in Parkinson's disease and related dopaminergic deficits. Front Syst Neurosci, 2014, 8: 45. DOI: 10.3389/fnsys.2014.00045

[44]

I. Rektorova, L. Krajcovicova, R. Marecek, et al. Effective connectivity of the default mode network in Parkinson's disease and Parkinson's disease dementia. Clin Neurophysiol, 2014, 125: S126-S127.

[45]

石源源，王天俊．静息态功能磁共振成像在帕金森病中的研究进展.中国全科医学, 2018, 21(14): 1757-1760. DOI: 10.12015

[46]

郭卫娜，李晶雪，常雅君．认知功能障碍的帕金森病患者脑静息态功能连接．放射学实践, 2020, 35(5): 682-686. DOI: 10.13609/j.cnki.1000-0313.2020.05.022

[47]

Rzepa E, McCabe C. Anhedonia and depression severity dissociated by dmPFC resting-state functional connectivity in adolescents. J Psychopharmacol, 2018, 32(10): 1067-1074. DOI: 10.1177/0269881118799935

[48]

Liang PP, Xu YC, Lan F. Decreased cerebral blood flow in mesial thalamus and Precuneus/PCC during Midazolam Induced Sedation Assessed with ASL. Neuroinformatics, 2018, 16(3-4): 403-410. DOI: 10.1007/s12021-018-9368-y

[49]

Wang XY, Margulies DS, Smallwood J. A gradient from long-term memory to novel cognition: transitions through default mode and executive cortex. NeuroImage, 2020, 220: 117074. DOI: 10.1101/2020.01.16.908327

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