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Advances in MRI study of brain structure and function changes and related factors of metabolic disorders in Parkinson's disease
LI Wanyao  DU Wei  MIAO Yanwei 

Cite this article as: Li WY, Du W, Miao YW. Advances in MRI study of brain structure and function changes and related factors of metabolic disorders in Parkinson's disease[J]. Chin J Magn Reson Imaging, 2022, 13(7): 138-142. DOI:10.12015/issn.1674-8034.2022.07.027.


[Abstract] Parkinson's disease (PD) is a progressive degenerative disease of the central nervous system, characterized by brain structural change and loss of function caused by neurodystrophy. Metabolic syndrome (MS) refers to a group of interrelated cerebrovascular disease risk factors that lead to insulin resistance. In recent years, more and more studies have shown that metabolic disorders can seriously affect the induction and progression of neurodegenerative diseases. MRI is a non-invasive technique to evaluate the changes of brain structure and function. This article reviews the progress of MRI research on changes in brain structure and function and metabolic disorders in patients with PD.
[Keywords] Parkinson's disease;metabolic syndrome;brain function;brain structure;magnetic resonance imaging

LI Wanyao   DU Wei   MIAO Yanwei*  

Department of Radiology, the First Affiliated Hospital of Dalian Medical University, Dalian 116011, China

Miao YW, E-mail: ywmiao716@163.com

Conflicts of interest   None.

Received  2022-01-26
Accepted  2022-06-22
DOI: 10.12015/issn.1674-8034.2022.07.027
Cite this article as: Li WY, Du W, Miao YW. Advances in MRI study of brain structure and function changes and related factors of metabolic disorders in Parkinson's disease[J]. Chin J Magn Reson Imaging, 2022, 13(7): 138-142.DOI:10.12015/issn.1674-8034.2022.07.027

[1]
Polo-Morales A, Alcocer-Salas A, Rodríguez-Violante M, et al. Association Between Somatization and Nonmotor Symptoms Severity in People With Parkinson Disease[J]. J Geriatr Psychiatry Neurol, 2021, 34(1): 60-65. DOI: 10.1177/0891988720901787.
[2]
Cuenca L, Gil-Martinez AL, Cano-Fernandez L, et al. Parkinson's disease: a short story of 200 years[J]. Histol Histopathol, 2019, 34(6): 573-591. DOI: 10.14670/HH-18-073.
[3]
Chung KK, Zhang Y, Lim KL, et al. Parkin ubiquitinates the alpha-synuclein-interacting protein, synphilin-1: implications for Lewy-body formation in Parkinson disease[J]. Nat Med, 2001, 7(10): 1144-1150. DOI: 10.1038/nm1001-1144.
[4]
Trist BG, Hare DJ, Double KL. Oxidative stress in the aging substantia nigra and the etiology of Parkinson's disease[J/OL]. Aging Cell, 2019, 18(6) [2022-01-26]. https://onlinelibrary.wiley.com/doi/10.1111/acel.13031. DOI: 10.1111/acel.13031.
[5]
Gentile F, Doneddu PE, Riva N, et al. Diet, Microbiota and Brain Health: Unraveling the Network Intersecting Metabolism and Neurodegeneration[J/OL]. Int J Mol Sci, 2020, 21(20) [2022-01-26]. https://www.mdpi.com/1422-0067/21/20/7471. DOI: 10.3390/ijms21207471.
[6]
Qin J, Li Y, Cai Z, et al. A metagenome-wide association study of gut microbiota in type 2 diabetes[J]. Nature, 2012, 490(7418): 55-60. DOI: 10.1038/nature11450.
[7]
Carrier A. Metabolic Syndrome and Oxidative Stress: A Complex Relationship[J]. Antioxid Redox Signal, 2017, 26(9): 429-431. DOI: 10.1089/ars.2016.6929.
[8]
Camandola S, Mattson MP. Brain metabolism in health, aging, and neurodegeneration[J]. EMBO J, 2017, 36(11): 1474-1492. DOI: 10.15252/embj.201695810.
[9]
Murakami Y, Kakeda S, Watanabe K, et al. Usefulness of quantitative susceptibility mapping for the diagnosis of Parkinson disease[J]. AJNR Am J Neuroradiol, 2015, 36(6): 1102-1108. DOI: 10.3174/ajnr.A4260.
[10]
He N, Ling H, Ding B, et al. Region-specific disturbed iron distribution in early idiopathic Parkinson's disease measured by quantitative susceptibility mapping[J]. Hum Brain Mapp, 2015, 36(11): 4407-4420. DOI: 10.1002/hbm.22928.
[11]
Guan X, Xuan M, Gu Q, et al. Regionally progressive accumulation of iron in Parkinson's disease as measured by quantitative susceptibility mapping[J/OL]. NMR Biomed, 2017, 30(4) [2022-01-26]. https://analyticalsciencejournals.onlinelibrary.wiley.com/doi/10.1002/nbm.3489. DOI: 10.1002/nbm.3489.
[12]
Li SJ, Ren YD, Li J, et al. The role of iron in Parkinson's disease monkeys assessed by susceptibility weighted imaging and inductively coupled plasma mass spectrometry[J/OL]. Life Sci, 2020, 240 [2022-01-26]. https://www.sciencedirect.com/science/article/abs/pii/S0024320519310185?via%3Dihub. DOI: 10.1016/j.lfs.2019.117091.
[13]
Ghassaban K, He N, Sethi SK, et al. Regional High Iron in the Substantia Nigra Differentiates Parkinson's Disease Patients From Healthy Controls[J/OL]. Front Aging Neurosci, 2019, 11 [2022-01-26]. https://www.frontiersin.org/articles/10.3389/fnagi.2019.00106/full. DOI: 10.3389/fnagi.2019.00106.
[14]
Martin-Bastida A, Lao-Kaim NP, Loane C, et al. Motor associations of iron accumulation in deep grey matter nuclei in Parkinson's disease: a cross-sectional study of iron-related magnetic resonance imaging susceptibility[J]. Eur J Neurol, 2017, 24(2): 357-365. DOI: 10.1111/ene.13208.
[15]
Gao BB, Miao YW, Tian SY, et al. SWI and DKI study of brain iron deposition and microstructure change in gray matter nucleus in Parkinson's disease[J]. Chin J Magn Reson Imaging, 2017, 8(12): 881-886. DOI: 10.12015/issn.1674-8034.2017.12.001.
[16]
Mochizuki H, Choong CJ, Baba K. Parkinson's disease and iron[J]. J Neural Transm (Vienna), 2020, 127(2): 181-187. DOI: 10.1007/s00702-020-02149-3.
[17]
Xuan M, Guan X, Gu Q, et al. Different iron deposition patterns in early- and middle-late-onset Parkinson's disease[J]. Parkinsonism Relat Disord, 2017, 44: 23-27. DOI: 10.1016/j.parkreldis.2017.08.013.
[18]
Blazejewska AI, Schwarz ST, Pitiot A, et al. Visualization of nigrosome 1 and its loss in PD: pathoanatomical correlation and in vivo 7T MRI[J]. Neurology, 2013, 81: 534-540. DOI: 10.1212/WNL.0000000000000398.
[19]
Calloni SF, Conte G, Sbaraini S, et al. Multiparametric MR imaging of Parkinsonisms at 3 tesla: Its role in the differentiation of idiopathic Parkinson's disease versus atypical Parkinsonian disorders[J]. Eur J Radiol, 2018, 109: 95-100. DOI: 10.1016/j.ejrad.2018.10.032.
[20]
Fedeli MP, Contarino VE, Siggillino S, et al. Iron deposition in Parkinsonisms: A Quantitative Susceptibility Mapping study in the deep grey matter[J/OL]. Eur J Radiol, 2020, 133 [2022-01-26]. https://www.ejradiology.com/article/S0720-048X(20)30584-2/fulltext. DOI: 10.1016/j.ejrad.2020.109394.
[21]
He N, Huang P, Ling H, et al. Dentate nucleus iron deposition is a potential biomarker for tremor-dominant Parkinson's disease[J/OL]. NMR Biomed, 2017, 30(4) [2022-01-26]. https://analyticalsciencejournals.onlinelibrary.wiley.com/doi/10.1002/nbm.3554. DOI: 10.1002/nbm.3554.
[22]
Shi L, Huang C, Luo Q, et al. The Association of Iron and the Pathologies of Parkinson's Diseases in MPTP/MPP+-Induced Neuronal Degeneration in Non-human Primates and in Cell Culture[J/OL]. Front Aging Neurosci, 2019, 11 [2022-01-26]. https://www.frontiersin.org/articles/10.3389/fnagi.2019.00215/full. DOI: 10.3389/fnagi.2019.00215.
[23]
An H, Zeng X, Niu T, et al. Quantifying iron deposition within the substantia nigra of Parkinson's disease by quantitative susceptibility mapping[J]. J Neurol Sci, 2018, 386: 46-52. DOI: 10.1016/j.jns.2018.01.008.
[24]
Guo XL, Geng CJ, Chen LH. Value of 3.0T magnetic resonance imaging plussusceptibility weighted imaging in evaluating basal ganglia volume in patients withParkinson's disease at different stages[J]. Journal of Clinical Medicine in Practice, 2021, 25(11): 18-21. DOI: 10.7619/jcmp.20211242.
[25]
Breen DP, Nombela C, Vuono R, et al. Hypothalamic volume loss is associated with reduced melatonin output in Parkinson's disease[J]. Mov Disord, 2016, 31(7): 1062-1066. DOI: 10.1002/mds.26592.
[26]
Crutcher MD, DeLong MR. Single cell studies of the primate putamen[J]. Exp Brain Res, 1984, 53(2): 233-243. DOI: 10.1007/bf00238153.
[27]
Hagiwara A, Warntjes M, Hori M, et al. SyMRI of the Brain: Rapid Quantification of Relaxation Rates and Proton Density, With Synthetic MRI, Automatic Brain Segmentation, and Myelin Measurement[J]. Invest Radiol, 2017, 52(10): 647-657. DOI: 10.1097/RLI.0000000000000365.
[28]
Honma M, Kuroda T, Futamura A, et al. Mental time dysfunction in Parkinson's and Alzheimer's diseases[J]. Brain Nerve, 2015, 67(3): 297-302. DOI: 10.11477/mf.1416200135.
[29]
Vriend C, Boedhoe PS, Rutten S, et al. A smaller amygdala is associated with anxiety in Parkinson's disease: a combined FreeSurfer-VBM study[J]. J Neurol Neurosurg Psychiatry, 2016, 87(5): 493-500. DOI: 10.1136/jnnp-2015-310383.
[30]
Bingbing G, Yujing Z, Yanwei M, et al. Diffusion Kurtosis Imaging of Microstructural Changes in Gray Matter Nucleus in Parkinson Disease[J/OL]. Front Neurol, 2020, 11 [2022-01-26]. https://www.frontiersin.org/articles/10.3389/fneur.2020.00252/full. DOI: 10.3389/fneur.2020.00252.
[31]
Khundrakpam BS, Lewis JD, Kostopoulos P, et al. Cortical Thickness Abnormalities in Autism Spectrum Disorders Through Late Childhood, Adolescence, and Adulthood: A Large-Scale MRI Study[J]. Cereb Cortex, 2017, 27(3): 1721-1731. DOI: 10.1093/cercor/bhx038.
[32]
Laansma MA, Bright JK, Al-Bachari S, et al. International Multicenter Analysis of Brain Structure Across Clinical Stages of Parkinson's Disease[J]. Mov Disord, 2021, 36(11): 2583-2594. DOI: 10.1002/mds.28706.
[33]
Zhang CQ. Quantitative analysis methods of brain structure and function in patients with early Parkinson's disease[D]. Qingdao: Shandong University of Science and Technology, 2019. DOI: 10.27275/d.cnki.gsdku.2019.000488.
[34]
Wilson H, Niccolini F, Pellicano C, et al. Cortical thinning across Parkinson's disease stages and clinical correlates[J]. J Neurol Sci, 2019, 398: 31-38. DOI: 10.1016/j.jns.2019.01.020.
[35]
Sampedro F, Marín-Lahoz J, Martínez-Horta S, et al. Dopaminergic degeneration induces early posterior cortical thinning in Parkinson's disease[J]. Neurobiol Dis, 2019, 124: 29-35. DOI: 10.1016/j.nbd.2018.11.001.
[36]
Zhang L, Wang M, Sterling NW, et al. Cortical Thinning and Cognitive Impairment in Parkinson's Disease without Dementia[J]. IEEE/ACM Trans Comput Biol Bioinform, 2018, 15(2): 570-580. DOI: 10.1109/TCBB.2015.2465951.
[37]
Rong S, Li Y, Li B, et al. Meynert nucleus-related cortical thinning in Parkinson's disease with mild cognitive impairment[J]. Quant Imaging Med Surg, 2021, 11(4): 1554-1566. DOI: 10.21037/qims-20-444.
[38]
Bergamino M, Keeling EG, Mishra VR, et al. Assessing White Matter Pathology in Early-Stage Parkinson Disease Using Diffusion MRI: A Systematic Review[J/OL]. Front Neurol, 2020, 11 [2022-01-26]. https://www.frontiersin.org/articles/10.3389/fneur.2020.00314/full. DOI: 10.3389/fneur.2020.00314.
[39]
Sanjari Moghaddam H, Dolatshahi M, Mohebi F, et al. Structural white matter alterations as compensatory mechanisms in Parkinson's disease: A systematic review of diffusion tensor imaging studies[J]. J Neurosci Res, 2020, 98(7): 1398-1416. DOI: 10.1002/jnr.24617.
[40]
Pelizzari L, Di Tella S, Laganà MM, et al. White matter alterations in early Parkinson's disease: role of motor symptom lateralization[J]. Neurol Sci, 2020, 41(2): 357-364. DOI: 10.1007/s10072-019-04084-y.
[41]
Chen C. DTI assessment of brain white matter structural changes in Parkinson's diseasepatients[D]. Zhengzhou: Zhengzhou University, 2019.
[42]
Gu Q, Huang P, Xuan M, et al. Greater loss of white matter integrity in postural instability and gait difficulty subtype of Parkinson's disease[J]. Can J Neurol Sci, 2014, 41(6): 763-768. DOI: 10.1017/cjn.2014.34.
[43]
Lewis SJ, Foltynie T, Blackwell AD, et al. Heterogeneity of Parkinson's disease in the early clinical stages using a data driven approach[J]. J Neurol Neurosurg Psychiatry, 2005, 76(3): 343-348. DOI: 10.1136/jnnp.2003.033530.
[44]
Li Z, Liu W, Xiao C, et al. Abnormal white matter microstructures in Parkinson's disease and comorbid depression: A whole-brain diffusion tensor imaging study[J/OL]. Neurosci Lett, 2020, 735 [2022-01-26]. https://linkinghub.elsevier.com/retrieve/pii/S0304394020305085. DOI: 10.1016/j.neulet.2020.135238.
[45]
Zarkali A, McColgan P, Leyland LA, et al. Fiber-specific white matter reductions in Parkinson hallucinations and visual dysfunction[J/OL]. Neurology, 2020, 94(14) [2022-01-26]. https://n.neurology.org/content/94/14/e1525. DOI: 10.1212/WNL.0000000000009014.
[46]
Bledsoe IO, Stebbins GT, Merkitch D, et al. White matter abnormalities in the corpus callosum with cognitive impairment in Parkinson disease[J/OL]. Neurology, 2018, 91(24) [2022-01-26]. https://n.neurology.org/content/91/24/e2244. DOI: 10.1212/WNL.0000000000006646.
[47]
Herrington TM, Briscoe J, Eskandar E. Structural and Functional Network Dysfunction in Parkinson Disease[J]. Radiology, 2017, 285(3): 725-727. DOI: 10.1148/radiol.247172401.
[48]
Wang S, Zhang Y, Lei J, et al. Investigation of sensorimotor dysfunction in Parkinson disease by resting-state fMRI[J/OL]. Neurosci Lett, 2021, 742 [2022-01-26]. https://linkinghub.elsevier.com/retrieve/pii/S0304394020307825. DOI: 10.1016/j.neulet.2020.135512.
[49]
Helmich RC. The cerebral basis of Parkinsonian tremor: A network perspective. Mov Disord, 2018, 33(2): 219-231. DOI: 10.1002/mds.27224.
[50]
Hepp DH, Foncke EMJ, Olde Dubbelink KTE, et al. Loss of Functional Connectivity in Patients with Parkinson Disease and Visual Hallucinations[J]. Radiology, 2017, 285(3): 896-903. DOI: 10.1148/radiol.2017170438.
[51]
Ji GJ, Hu P, Liu TT, et al. Functional Connectivity of the Corticobasal Ganglia-Thalamocortical Network in Parkinson Disease: A Systematic Review and Meta-Analysis with Cross-Validation[J]. Radiology, 2018, 287(3): 973-982. DOI: 10.1148/radiol.2018172183.
[52]
Maiti B, Koller JM, Snyder AZ, et al. Cognitive correlates of cerebellar resting-state functional connectivity in Parkinson disease[J/OL]. Neurology, 2020, 94(4) [2022-01-26]. https://n.neurology.org/content/94/4/e384. DOI: 10.1212/WNL.0000000000008754.
[53]
Wang M, Liao H, Shen Q, et al. Changed Resting-State Brain Signal in Parkinson's Patients With Mild Depression[J/OL]. Frontiers in Neurology, 2020, 11 [2022-01-26]. https://www.frontiersin.org/articles/10.3389/fneur.2020.00028/full. DOI: 10.3389/fneur.2020.00028.
[54]
Syrimi ZJ, Vojtisek L, Eliasova I, et al. Arterial spin labelling detects posterior cortical hypoperfusion in non-demented patients with Parkinson's disease[J]. J Neural Transm, 2017, 124 (5): 551-557. DOI: 10.1007/s00702-017-1703-1.
[55]
Pelizzari L, Laganà MM, Di TS, et al. Combined Assessment of Diffusion Parameters and Cerebral Blood Flow Within Basal Ganglia in Early Parkinson's Disease[J]. Front Aging Neurosci, 2019, 11: 134. DOI: 10.3389/fnagi.2019.00134.
[56]
Wei XB, Yan RH, Chen ZY, et al. Combined Diffusion Tensor Imaging and Arterial Spin Labeling as Markers of Early Parkinson's disease[J/OL]. Sci Rep, 2016, 6 [2022-01-26]. https://www.nature.com/articles/srep33762. DOI: 10.1038/srep33762.
[57]
Nam GE, Kim SM, Han K, et al. Metabolic syndrome and risk of Parkinson disease: A nationwide cohort study[J/OL]. PLoS Med, 2018, 15(8) [2022-01-26]. https://journals.plos.org/plosmedicine/article?id=10.1371/journal.pmed.1002640. DOI: 10.1371/journal.pmed.1002640.
[58]
de Bem AF, Krolow R, Farias HR, et al. Animal Models of Metabolic Disorders in the Study of Neurodegenerative Diseases: An Overview[J/OL]. Front Neurosci, 2020, 14 [2022-01-26]. https://www.frontiersin.org/articles/10.3389/fnins.2020.604150/full. DOI: 10.3389/fnins.2020.604150.
[59]
de A Boleti AP, Almeida JA, Migliolo L. Impact of the metabolic syndrome on the evolution of neurodegenerative diseases[J]. Neural Regen Res, 2021, 16(4): 688-689. DOI: 10.4103/1673-5374.295329.
[60]
Alecu I, Bennett SAL. Dysregulated Lipid Metabolism and Its Role in α-Synucleinopathy in Parkinson's Disease[J/OL]. Front Neurosci, 2019, 13 [2022-01-26]. https://www.frontiersin.org/articles/10.3389/fnins.2019.00328/full. DOI: 10.3389/fnins.2019.00328.
[61]
Rahmani J, Roudsari AH, Bawadi H, et al. Body mass index and risk of Parkinson, Alzheimer, Dementia, and Dementia mortality: a systematic review and dose-response meta-analysis of cohort studies among 5 million participants[J]. Nutr Neurosci, 2020, 25(3): 425-431. DOI: 10.1080/1028415X.2020.1758888.
[62]
Roos E, Grotta A, Yang F, et al. Body mass index, sitting time, and risk of Parkinson disease[J/OL]. Neurology, 2018, 90(16) [2022-01-26]. https://n.neurology.org/content/90/16/e1413. DOI: 10.1212/WNL.0000000000005328.
[63]
Hu G, Jousilahti P, Nissinen A, et al. Body mass index and the risk of Parkinson disease[J]. Neurology, 2006, 67(11): 1955-1959. DOI: 10.1212/01.wnl.0000247052.18422.e5.
[64]
Kyrozis A, Ghika A, Stathopoulos P, et al. Dietary and lifestyle variables in relation to incidence of Parkinson's disease in Greece[J]. Eur J Epidemiol, 2013, 28(1): 67-77. DOI: 10.1007/s10654-012-9760-0.
[65]
Jeong SM, Han K, Kim D, et al. Body mass index, diabetes, and the risk of Parkinson's disease[J]. Mov Disord, 2020, 35(2): 236-244. DOI: 10.1002/mds.27922.
[66]
Abbott RD, Ross GW, White LR, et al. Midlife adiposity and the future risk of Parkinson's disease[J]. Neurology, 2002, 59(7): 1051-1057. DOI: 10.1212/wnl.59.7.1051.
[67]
Muddapu VR, Dharshini SAP, Chakravarthy VS, et al. Neurodegenerative Diseases-Is Metabolic Deficiency the Root Cause?[J/OL]. Front Neurosci, 2020, 14 [2022-01-26]. https://www.frontiersin.org/articles/10.3389/fnins.2020.00213/full. DOI: 10.3389/fnins.2020.00213.
[68]
Yin F, Boveris A, Cadenas E. Mitochondrial energy metabolism and redox signaling in brain aging and neurodegeneration[J]. Antioxid Redox Signal, 2014, 20(2): 353-71. DOI: 10.1089/ars.2012.4774.
[69]
Hoyer S. The young-adult and normally aged brain. Its blood flow and oxidative metabolism. A review—part I[J]. Arch Gerontol Geriatr, 1982, 1(2): 101-116. DOI: 10.1016/0167-4943(82)90010-3..
[70]
Borghammer P, Chakravarty M, Jonsdottir KY, et al. Cortical hypometabolism and hypoperfusion in Parkinson's disease is extensive: probably even at early disease stages[J]. Brain Struct Funct, 2014: 303-317. DOI: 10.1007/s00429-010-0246-0.
[71]
Dunn L, Allen GF, Mamais A, et al. Dysregulation of glucose metabolism is an early event in sporadic Parkinson's disease[J]. Neurobiol Aging, 2014, 35(5): 1111-1115. DOI: 10.1016/j.neurobiolaging.2013.11.001.
[72]
Yang YW, Hsieh TF, Li CI, et al. Increased risk of Parkinson disease with diabetes mellitus in a population-based study[J/OL]. Medicine (Baltimore), 2017, 96(3) [2022-01-26]. https://journals.lww.com/md-journal/Fulltext/2017/01200/Increased_risk_of_Parkinson_disease_with_diabetes.30.aspx. DOI: 10.1097/MD.0000000000005921.
[73]
Pagano G, Polychronis S, Wilson H, et al. Diabetes mellitus and Parkinson disease[J/OL]. Neurology, 2018, 90(19) [2022-01-26]. https://n.neurology.org/content/90/19/e1654. DOI: 10.1212/WNL.0000000000005475.
[74]
Santiago JA, Potashkin JA. Shared dysregulated pathways lead to Parkinson's disease and diabetes[J]. Trends Mol Med, 2013, 19(3): 176-186. DOI: 10.1016/j.molmed.2013.01.002.
[75]
Simon KC, Chen H, Schwarzschild M, et al. Hypertension, hypercholesterolemia, diabetes, and risk of Parkinson disease[J]. Neurology, 2007, 69(17): 1688-1695. DOI: 10.1212/01.wnl.0000271883.45010.8a.
[76]
Ascherio A, Schwarzschild MA. The epidemiology of Parkinson's disease: risk factors and prevention[J]. Lancet Neurol, 2016, 15(12): 1257-1272. DOI: 10.1016/S1474-4422(16)30230-7.
[77]
Fu X, Wang Y, He X, et al. A systematic review and meta-analysis of serum cholesterol and triglyceride levels in patients with Parkinson's disease[J]. Lipids Health Dis, 2020, 19(1): 97. DOI: 10.1186/s12944-020-01284-w.
[78]
Huang X, Auinger P, Eberly S, et al. Serum cholesterol and the progression of Parkinson's disease: results from DATATOP[J/OL]. PLoS One, 2011, 6(8) [2022-01-26]. https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0022854. DOI: 10.1371/journal.pone.0022854.
[79]
Du G, Lewis MM, Shaffer ML, et al. Serum cholesterol and nigrostriatal R2* values in Parkinson's disease[J/OL]. PLoS One, 2012, 7(4) [2022-01-26]. https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0035397. DOI: 10.1371/journal.pone.0035397.
[80]
Paul R, Choudhury A, Borah A. Cholesterol—A putative endogenous contributor towards Parkinson's disease[J]. Neurochem Int, 2015, 90: 125-133. DOI: 10.1016/j.neuint.2015.07.025.
[81]
Paul R, Choudhury A, Kumar S, et al. Cholesterol contributes to dopamine-neuronal loss in MPTP mouse model of Parkinson's disease: Involvement of mitochondrial dysfunctions and oxidative stress[J/OL]. PLoS One, 2017, 12(2) [2022-01-26]. https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0171285. DOI: 10.1371/journal.pone.0171285.
[82]
Liu Z, Fan Q, Wu S, et al. Compared with the monocyte to high-density lipoprotein ratio (MHR) and the neutrophil to lymphocyte ratio (NLR), the neutrophil to high-density lipoprotein ratio (NHR) is more valuable for assessing the inflammatory process in Parkinson's disease[J]. Lipids Health Dis, 2021, 20(1): 35. DOI: 10.1186/s12944-021-01462-4.
[83]
Bahrami A, Barreto GE, Lombardi G, et al. Emerging roles for high-density lipoproteins in neurodegenerative disorders[J]. Biofactors, 2019, 45(5): 725-739. DOI: 10.1002/biof.1541.
[84]
Gillies GE, McArthur S. Estrogen actions in the brain and the basis for differential action in men and women: a case for sex-specific medicines[J]. Pharmacol Rev, 2010, 62(2): 155-198. DOI: 10.1124/pr.109.002071.
[85]
Sakuta H, Suzuki K, Miyamoto T, et al. Serum uric acid levels in Parkinson's disease and related disorders[J/OL]. Brain Behav, 2017, 7(1) [2022-01-26]. https://onlinelibrary.wiley.com/doi/10.1002/brb3.598. DOI: 10.1002/brb3.598.
[86]
Moccia M, Pappatà S, Erro R, et al. Uric acid relates to dopamine transporter availability in Parkinson's disease[J]. Acta Neurol Scand, 2015, 131(2): 127-131. DOI: 10.1111/ane.12295.
[87]
Wen M, Zhou B, Chen YH, et al. Serum uric acid levels in patients with Parkinson's disease: A meta-analysis[J/OL]. PLoS One, 2017, 12(3) [2022-01-26]. https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0173731. DOI: 10.1371/journal.pone.0173731.
[88]
Petrou M, Davatzikos C, Hsieh M, et al. Diabetes, Gray Matter Loss, and Cognition in the Setting of Parkinson Disease[J]. Acad Radiol, 2016, 23(5): 577-581. DOI: 10.1016/j.acra.2015.07.014.
[89]
Ong M, Foo H, Chander RJ, et al. Influence of diabetes mellitus on longitudinal atrophy and cognition in Parkinson's disease[J]. J Neurol Sci, 2017, 377: 122-126. DOI: 10.1016/j.jns.2017.04.010.

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