AccScience Publishing / AN / Online First / DOI: 10.36922/an.1683
REVIEW

Inflammation in ischemic stroke patients with type 2 diabetes – Part I: Atherosclerosis formation, acute ischemia, post-stroke infection, and long-term sequelae

Liqun Zhang1* Ying Chen2,3 Jingxian Xu2,3 Christopher P. Corpe4 Anan Shtaya5 Philip Benjamin6 Yun Xu2,3,7,8,9
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1 Department of Neurology, St George’s University Hospital, London, United Kingdom
2 Department of Neurology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, Jiangsu, China
3 Department of Neurology, Nanjing Drum Tower Hospital, State Key Laboratory of Pharmaceutical Biotechnology and Institute of Translational Medicine for Brain Critical Diseases, Nanjing University, Nanjing, Jiangsu, China
4 Department of Nutritional Sciences, School of Life Courses and Population Sciences, King’s College London, London, United Kingdom
5 Head of Neuroscience at Arab Hospitals Group, Ramallah, Palestine
6 Department of Neuroradiology, St George’s University Hospital, London, United Kingdom
7 Jiangsu Key Laboratory for Molecular Medicine, Medical School of Nanjing University, Nanjing, Jiangsu, China
8 Jiangsu Provincial Key Discipline of Neurology, Nanjing, Jingasu, China
9 Nanjing Neurology Medical Center, Nanjing, Jinagsu, China
Advanced Neurology 2024, 3(2), 1683 https://doi.org/10.36922/an.1683
Submitted: 26 August 2023 | Accepted: 27 February 2024 | Published: 4 June 2024
(This article belongs to the Special Issue Advances in stroke research and therapy)
© 2024 by the Author(s). This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution 4.0 International License ( https://creativecommons.org/licenses/by/4.0/ )
Abstract

Stroke is the leading cause of disability and the second leading cause of death worldwide. Diabetes mellitus is a critical independent cardiovascular risk factor in patients, irrespective of age, smoking, and hypertension. Approximately one-third of first-time ischemic stroke patients have diabetes. Inflammation is among the most important pathological mechanisms in atheroma formation, the damage cascades of the acute phase, as well as during the subacute and chronic phases after stroke. Diabetes, as a common risk factor for stroke, is often present for a long time before a stroke occurs, causing low-grade inflammation, and disrupting the proper functioning of the neurovascular units. These proinflammatory processes and maladaptive immune mechanisms are further accelerated after cerebral ischemia and worsen the stroke outcome in diabetic patients. Clinical treatments for ischemic stroke are currently focused on restoring cerebral blood flow (reperfusion) in the acute phase, including thrombolysis and mechanical thrombectomy, which are not applicable to patients that fall outside of the treatment window and/or without large-vessel occlusion. There are few approved treatments targeting cellular injury caused by inflammation. There are even fewer data on effective treatment for diabetic stroke targeting inflammation. This paper presents the first part of a review focusing on the temporospatial aspects of inflammation in ischemic stroke pathophysiology in stroke patients with type 2 diabetes.

Keywords
Stroke
Diabetes
Inflammation
Immune
Pathophysiology
Therapeutics
Funding
None.
References
  1. GBD 2016 Lifetime Risk of Stroke Collaborators, Feigin VL, Nguyen G, et al. Global, regional, and country-specific lifetime risks of stroke, 1990 and 2016. N Engl J Med. 2018;379(25):2429-2437. doi: 10.1056/NEJMoa1804492

 

  1. Emerging Risk Factors Collaboration, Sarwar N, Gao P, et al. Diabetes mellitus, fasting blood glucose concentration, and risk of vascular disease: A collaborative meta-analysis of 102 prospective studies. Lancet. 2010;375(9733):2215-2222. doi: 10.1016/S0140-6736(10)60484-9

 

  1. Soriano-Reixach MM, Vivanco-Hidalgo RM, Ois A, Rodriguez-Campello A, Roquer J. Interaction of sex and diabetes on outcome after ischemic stroke. Front Neurol. 2018;9:250. doi: 10.3389/fneur.2018.00250

 

  1. Available from: https://www.cdc.gov/diabetes/basics/quick-facts.html

 

  1. Ogurtsova K, da Rocha Fernandes JD, Huang Y, et al. IDF diabetes atlas: Global estimates for the prevalence of diabetes for 2015 and 2040. Diabetes Res Clin Pract. 2017;128:40-50. doi: 10.1016/j.diabres.2017.03.024

 

  1. Lloyd-Jones D, Adams R, Carnethon M, et al. Heart disease and stroke statistics--2009 update: A report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation. 2009;119(3):e21-e181. doi: 10.1161/CIRCULATIONAHA.108.191261

 

  1. Deb P, Sharma S, Hassan KM. Pathophysiologic mechanisms of acute ischemic stroke: An overview with emphasis on therapeutic significance beyond thrombolysis. Pathophysiology. 2010;17(3):197-218. doi: 10.1016/j.pathophys.2009.12.001

 

  1. Iadecola C, Buckwalter MS, Anrather J. Immune responses to stroke: Mechanisms, modulation, and therapeutic potential. J Clin Invest. 2020;130(6):2777-2788. doi: 10.1172/JCI135530

 

  1. Mulnier HE, Seaman HE, Raleigh VS, et al. Risk of stroke in people with type 2 diabetes in the UK: A study using the general practice research database. Diabetologia. 2006;49(12):2859-2865. doi: 10.1007/s00125-006-0493-z

 

  1. Jebari-Benslaiman S, Galicia-Garcia U, Larrea-Sebal A, et al. Pathophysiology of atherosclerosis. Int J Mol Sci. 2022;23(6):3346. doi: 10.3390/ijms23063346

 

  1. Libby P. The changing landscape of atherosclerosis. Nature. 2021;592(7855):524-533. doi: 10.1038/s41586-021-03392-8

 

  1. Liu T, Zhang L, Joo D, Sun SC. NF-kappaB signaling in inflammation. Signal Transduct Target Ther. 2017;2:17023. doi: 10.1038/sigtrans.2017.23

 

  1. Bentzon JF, Otsuka F, Virmani R, Falk E. Mechanisms of plaque formation and rupture. Circ Res. 2014;114(12):1852-1866. doi: 10.1161/CIRCRESAHA.114.302721

 

  1. Mao R, Zong N, Hu Y, Chen Y, Xu Y. Neuronal death mechanisms and therapeutic strategy in ischemic stroke. Neurosci Bull. 2022;38(10):1229-1247. doi: 10.1007/s12264-022-00859-0

 

  1. Sabitha Vadakedath VK. Role of advanced glycation end products (AGE) in health and disease: An overview. Biochem Physiol. 2018;7:246. doi: 10.4172/2168-9652.1000246

 

  1. Knott HM, Brown BE, Davies MJ, Dean RT. Glycation and glycoxidation of low-density lipoproteins by glucose and low-molecular mass aldehydes. Formation of modified and oxidized particles. Eur J Biochem. 2003;270(17):3572-3582. doi: 10.1046/j.1432-1033.2003.03742.x

 

  1. Kheniser KG, Kashyap SR, Kasumov T. A systematic review: The appraisal of the effects of metformin on lipoprotein modification and function. Obes Sci Pract. 2019;5(1):36-45. doi: 10.1002/osp4.309

 

  1. Indyk D, Bronowicka-Szydelko A, Gamian A, Kuzan A. Advanced glycation end products and their receptors in serum of patients with type 2 diabetes. Sci Rep. 2021;11(1):13264. doi: 10.1038/s41598-021-92630-0

 

  1. Shu M, Cheng W, Jia X, et al. AGEs promote atherosclerosis by increasing LDL transcytosis across endothelial cells via RAGE/NF-kappaB/Caveolin-1 pathway. Mol Med. 2023;29(1):113. doi: 10.1186/s10020-023-00715-5

 

  1. Yu W, Tao M, Zhao Y, Hu X, Wang M. 4’-methoxyresveratrol alleviated AGE-induced inflammation via RAGE-mediated NF-kappaB and NLRP3 inflammasome pathway. Molecules. 2018;23(6):1447. doi: 10.3390/molecules23061447

 

  1. Chawla D, Bansal S, Banerjee BD, Madhu SV, Kalra OP, Tripathi AK. Role of advanced glycation end product (AGE)-induced receptor (RAGE) expression in diabetic vascular complications. Microvasc Res. 2014;95:1-6. doi: 10.1016/j.mvr.2014.06.010

 

  1. Da Veiga GL, Della Nina Raffo MG, da Costa Aguiar Alves B, Bacci MR, Fonseca FLA. NF-κB gene expression in peripheral blood and urine in early diagnosis of diabetic nephropathy - A liquid biopsy approach. Urine. 2019;1:24-28. doi: 10.1016/j.urine.2020.05.005

 

  1. Gromotowicz-Poplawska A, Kloza M, Aleksiejczuk M, et al. Nitric oxide as a modulator in platelet- and endothelium-dependent antithrombotic effect of eplerenone in diabetic rats. J Physiol Pharmacol. 2019;70(2). doi: 10.26402/jpp.2019.2.02

 

  1. Jamwal S, Sharma S. Vascular endothelium dysfunction: A conservative target in metabolic disorders. Inflamm Res. 2018;67(5):391-405. doi: 10.1007/s00011-018-1129-8

 

  1. Tejero J, Shiva S, Gladwin MT. Sources of vascular nitric oxide and reactive oxygen species and their regulation. Physiol Rev. 2019;99(1):311-379. doi: 10.1152/physrev.00036.2017

 

  1. Stefano GB, Challenger S, Kream RM. Hyperglycemia-associated alterations in cellular signaling and dysregulated mitochondrial bioenergetics in human metabolic disorders. Eur J Nutr. 2016;55(8):2339-2345. doi: 10.1007/s00394-016-1212-2

 

  1. Brownlee M. Biochemistry and molecular cell biology of diabetic complications. Nature. 2001;414(6865):813-820. doi: 10.1038/414813a

 

  1. Juge-Aubry CE, Henrichot E, Meier CA. Adipose tissue: A regulator of inflammation. Best Pract Res Clin Endocrinol Metab. 2005;19(4):547-566. doi: 10.1016/j.beem.2005.07.009

 

  1. Bidulescu A, Dinh PC Jr., Sarwary S, et al. Associations of leptin and adiponectin with incident type 2 diabetes and interactions among African Americans: The Jackson heart study. BMC Endocr Disord. 2020;20(1):31. doi: 10.1186/s12902-020-0511-z

 

  1. Hukshorn CJ, Saris WH. Leptin and energy expenditure. Curr Opin Clin Nutr Metab Care. 2004;7(6):629-633. doi: 10.1097/00075197-200411000-00007

 

  1. Saxton RA, Caveney NA, Moya-Garzon MD, et al. Structural insights into the mechanism of leptin receptor activation. Nat Commun. 2023;14(1):1797. doi: 10.1038/s41467-023-37169-6

 

  1. Raman P, Khanal S. Leptin in atherosclerosis: Focus on macrophages, endothelial and smooth muscle cells. Int J Mol Sci. 2021;22(11):5446. doi: 10.3390/ijms22115446

 

  1. Dong Z, Zhuang Q, Ye X, et al. Adiponectin inhibits NLRP3 inflammasome activation in nonalcoholic steatohepatitis via AMPK-JNK/ErK1/2-NFκB/ROS signaling pathways. Front Med (Lausanne). 2020;7:546445. doi: 10.3389/fmed.2020.546445

 

  1. Begum M, Choubey M, Tirumalasetty MB, et al. Adiponectin: A promising target for the treatment of diabetes and its complications. Life (Basel). 2023;13(11):2213. doi: 10.3390/life13112213

 

  1. Gindri Dos Santos B, Goedeke L. Macrophage immunometabolism in diabetes-associated atherosclerosis. Immunometabolism (Cobham). 2023;5(4):e00032. doi: 10.1097/IN9.0000000000000032

 

  1. Nagareddy PR, Murphy AJ, Stirzaker RA, et al. Hyperglycemia promotes myelopoiesis and impairs the resolution of atherosclerosis. Cell Metab. 2013;17(5):695-708. doi: 10.1016/j.cmet.2013.04.001

 

  1. Flynn MC, Kraakman MJ, Tikellis C, et al. Transient intermittent hyperglycemia accelerates atherosclerosis by promoting myelopoiesis. Circ Res. 2020;127(7):877-892. doi: 10.1161/CIRCRESAHA.120.316653

 

  1. Kanter JE, Hsu CC, Bornfeldt KE. Monocytes and macrophages as protagonists in vascular complications of diabetes. Front Cardiovasc Med. 2020;7:10. doi: 10.3389/fcvm.2020.00010

 

  1. Kaur R, Kaur M, Singh J. Endothelial dysfunction and platelet hyperactivity in type 2 diabetes mellitus: Molecular insights and therapeutic strategies. Cardiovasc Diabetol. 2018;17(1):121. doi: 10.1186/s12933-018-0763-3

 

  1. Dirnagl U, Iadecola C, Moskowitz MA. Pathobiology of ischaemic stroke: An integrated view. Trends Neurosci. 1999;22(9):391-397. doi: 10.1016/s0166-2236(99)01401-0

 

  1. Hartings JA, Rolli ML, Lu XC, Tortella FC. Delayed secondary phase of peri-infarct depolarizations after focal cerebral ischemia: Relation to infarct growth and neuroprotection. J Neurosci. 2003;23(37):11602-11610. doi: 10.1523/JNEUROSCI.23-37-11602.2003

 

  1. Saeed SA, Shad KF, Saleem T, Javed F, Khan MU. Some new prospects in the understanding of the molecular basis of the pathogenesis of stroke. Exp Brain Res. 2007;182(1):1-10. doi: 10.1007/s00221-007-1050-9

 

  1. Gulke E, Gelderblom M, Magnus T. Danger signals in stroke and their role on microglia activation after ischemia. Ther Adv Neurol Disord. 2018;11:1756286418774254. doi: 10.1177/1756286418774254

 

  1. Poznyak AV, Melnichenko AA, Wetzker R, Gerasimova EV, Orekhov AN. NLPR3 inflammasomes and their significance for atherosclerosis. Biomedicines. 2020;8(7):205. doi: 10.3390/biomedicines8070205

 

  1. Bellut M, Papp L, Bieber M, Kraft P, Stoll G, Schuhmann MK. NLPR3 inflammasome inhibition alleviates hypoxic endothelial cell death in vitro and protects blood-brain barrier integrity in murine stroke. Cell Death Dis. 2021;13(1):20. doi: 10.1038/s41419-021-04379-z

 

  1. Hong P, Gu RN, Li FX, et al. NLRP3 inflammasome as a potential treatment in ischemic stroke concomitant with diabetes. J Neuroinflammation. 2019;16(1):121. doi: 10.1186/s12974-019-1498-0

 

  1. Przykaza L. Understanding the connection between common stroke comorbidities, their associated inflammation, and the course of the cerebral Ischemia/Reperfusion cascade. Front Immunol. 2021;12:782569. doi: 10.3389/fimmu.2021.782569

 

  1. Franke M, Bieber M, Kraft P, Weber ANR, Stoll G, Schuhmann MK. The NLRP3 inflammasome drives inflammation in ischemia/reperfusion injury after transient middle cerebral artery occlusion in mice. Brain Behav Immun. 2021;92:223-233. doi: 10.1016/j.bbi.2020.12.009

 

  1. Cai Y, Leng S, Ma Y, Xu T, Chang D, Ju S. Dynamic change of MMP-9 in diabetic stroke visualized by optical imaging and treated with CD28 superagonist. Biomater Sci. 2021;9(7):2562-2570. doi: 10.1039/d0bm02014a

 

  1. Ravanan P, Srikumar IF, Talwar P. Autophagy: The spotlight for cellular stress responses. Life Sci. 2017;188:53-67. doi: 10.1016/j.lfs.2017.08.029

 

  1. Mo Y, Sun YY, Liu KY. Autophagy and inflammation in ischemic stroke. Neural Regen Res. 2020;15(8):1388-1396. doi: 10.4103/1673-5374.274331

 

  1. He J, Liu J, Huang Y, Tang X, Xiao H, Hu Z. Oxidative stress, inflammation, and autophagy: Potential targets of mesenchymal stem cells-based therapies in ischemic stroke. Front Neurosci. 2021;15:641157. doi: 10.3389/fnins.2021.641157

 

  1. O’Connell GC, Tennant CS, Lucke-Wold N, et al. Monocyte-lymphocyte cross-communication via soluble CD163 directly links innate immune system activation and adaptive immune system suppression following ischemic stroke. Sci Rep. 2017;7(1):12940. doi: 10.1038/s41598-017-13291-6

 

  1. Kim E, Tolhurst AT, Cho S. Deregulation of inflammatory response in the diabetic condition is associated with increased ischemic brain injury. J Neuroinflammation. 2014;11:83. doi: 10.1186/1742-2094-11-83

 

  1. Bemeur C, Ste-Marie L, Montgomery J. Increased oxidative stress during hyperglycemic cerebral ischemia. Neurochem Int. 2007;50(7-8):890-904. doi: 10.1016/j.neuint.2007.03.002

 

  1. Louiselle AE, Niemiec SM, Zgheib C, Liechty KW. Macrophage polarization and diabetic wound healing. Transl Res. 2021;236:109-116. doi: 10.1016/j.trsl.2021.05.006

 

  1. Bemeur C, Ste-Marie L, Desjardins P, et al. Dehydroascorbic acid normalizes several markers of oxidative stress and inflammation in acute hyperglycemic focal cerebral ischemia in the rat. Neurochem Int. 2005;46(5):399-407. doi: 10.1016/j.neuint.2004.11.007

 

  1. Ste-Marie L, Hazell AS, Bemeur C, Butterworth R, Montgomery J. Immunohistochemical detection of inducible nitric oxide synthase, nitrotyrosine and manganese superoxide dismutase following hyperglycemic focal cerebral ischemia. Brain Res. 2001;918(1-2):10-19. doi: 10.1016/s0006-8993(01)02903-1

 

  1. Li PA, Shuaib A, Miyashita H, He QP, Siesjo BK, Warner DS. Hyperglycemia enhances extracellular glutamate accumulation in rats subjected to forebrain ischemia. Stroke. 2000;31(1):183-192. doi: 10.1161/01.str.31.1.183

 

  1. Wicha P, Das S, Mahakkanukrauh P. Blood-brain barrier dysfunction in ischemic stroke and diabetes: The underlying link, mechanisms and future possible therapeutic targets. Anat Cell Biol. 2021;54(2):165-177. doi: 10.5115/acb.20.290

 

  1. Westendorp WF, Nederkoorn PJ, Vermeij JD, Dijkgraaf MG, van de Beek D. Post-stroke infection: A systematic review and meta-analysis. BMC Neurol. 2011;11:110. doi: 10.1186/1471-2377-11-110

 

  1. Suda S, Aoki J, Shimoyama T, et al. Stroke-associated infection independently predicts 3-month poor functional outcome and mortality. J Neurol. 2018;265(2):370-375. doi: 10.1007/s00415-017-8714-6

 

  1. Courties G, Herisson F, Sager HB, et al. Ischemic stroke activates hematopoietic bone marrow stem cells. Circ Res. 2015;116(3):407-417. doi: 10.1161/CIRCRESAHA.116.305207

 

  1. Roth S, Cao J, Singh V, et al. Post-injury immunosuppression and secondary infections are caused by an AIM2 inflammasome-driven signaling cascade. Immunity. 2021;54(4):648-659.e8. doi: 10.1016/j.immuni.2021.02.004

 

  1. Wang H, Deng QW, Peng AN, et al. β-arrestin2 functions as a key regulator in the sympathetic-triggered immunodepression after stroke. J Neuroinflammation. 2018;15(1):102. doi: 10.1186/s12974-018-1142-4

 

  1. Jiang C, Kong W, Wang Y, et al. Changes in the cellular immune system and circulating inflammatory markers of stroke patients. Oncotarget. 2017;8(2):3553-3567. doi: 10.18632/oncotarget.12201

 

  1. Simats A, Liesz A. Systemic inflammation after stroke: Implications for post-stroke comorbidities. EMBO Mol Med. 2022;14(9):e16269. doi: 10.15252/emmm.202216269

 

  1. Romer C, Engel O, Winek K, et al. Blocking stroke-induced immunodeficiency increases CNS antigen-specific autoreactivity but does not worsen functional outcome after experimental stroke. J Neurosci. 2015;35(20):7777-7794. doi: 10.1523/JNEUROSCI.1532-14.2015

 

  1. Berbudi A, Rahmadika N, Tjahjadi AI, Ruslami R. Type 2 diabetes and its impact on the immune system. Curr Diabetes Rev. 2020;16(5):442-449. doi: 10.2174/1573399815666191024085838

 

  1. Martinez N, Ketheesan N, Martens GW, West K, Lien E, Kornfeld H. Defects in early cell recruitment contribute to the increased susceptibility to respiratory Klebsiella pneumoniae infection in diabetic mice. Microbes Infect. 2016;18(10):649-655. doi: 10.1016/j.micinf.2016.05.007

 

  1. Gupta S, Maratha A, Siednienko J, et al. Analysis of inflammatory cytokine and TLR expression levels in Type 2 Diabetes with complications. Sci Rep. 2017;7(1):7633. doi: 10.1038/s41598-017-07230-8

 

  1. Mooradian AD, Reed RL, Meredith KE, Scuderi P. Serum levels of tumor necrosis factor and IL-1 alpha and IL-1 beta in diabetic patients. Diabetes Care. 1991;14(1):63-65. doi: 10.2337/diacare.14.1.63

 

  1. Tessaro FHG, Ayala TS, Nolasco EL, Bella LM, Martins JO. Insulin influences LPS-induced TNF-alpha and IL-6 release through distinct pathways in mouse macrophages from different compartments. Cell Physiol Biochem. 2017;42(5):2093-2104. doi: 10.1159/000479904

 

  1. Liu HF, Zhang HJ, Hu QX, et al. Altered polarization, morphology, and impaired innate immunity germane to resident peritoneal macrophages in mice with long-term type 2 diabetes. J Biomed Biotechnol. 2012;2012:867023. doi: 10.1155/2012/867023

 

  1. Restrepo BI, Twahirwa M, Rahbar MH, Schlesinger LS. Phagocytosis via complement or Fc-gamma receptors is compromised in monocytes from type 2 diabetes patients with chronic hyperglycemia. PLoS One. 2014;9(3):e92977. doi: 10.1371/journal.pone.0092977

 

  1. Schepers VP, Visser-Meily AM, Ketelaar M, Lindeman E. Poststroke fatigue: Course and its relation to personal and stroke-related factors. Arch Phys Med Rehabil. 2006;87(2):184-188. doi: 10.1016/j.apmr.2005.10.005

 

  1. Christensen D, Johnsen SP, Watt T, Harder I, Kirkevold M, Andersen G. Dimensions of post-stroke fatigue: A two-year follow-up study. Cerebrovasc Dis. 2008;26(2):134-141. doi: 10.1159/000139660

 

  1. Alghamdi I, Ariti C, Williams A, Wood E, Hewitt J. Prevalence of fatigue after stroke: A systematic review and meta-analysis. Eur Stroke J. 2021;6(4):319-332. doi: 10.1177/23969873211047681

 

  1. Hackett ML, Pickles K. Part I: Frequency of depression after stroke: An updated systematic review and meta-analysis of observational studies. Int J Stroke. 2014;9(8):1017-1025. doi: 10.1111/ijs.12357

 

  1. Roerink ME, van der Schaaf ME, Dinarello CA, Knoop H, van der Meer JW. Interleukin-1 as a mediator of fatigue in disease: A narrative review. J Neuroinflammation. 2017;14(1):16. doi: 10.1186/s12974-017-0796-7

 

  1. Fang M, Zhong L, Jin X, et al. Effect of inflammation on the process of stroke rehabilitation and poststroke depression. Front Psychiatry. 2019;10:184. doi: 10.3389/fpsyt.2019.00184

 

  1. Hu Y, Zheng Y, Wu Y, Ni B, Shi S. Imbalance between IL-17A-producing cells and regulatory T cells during ischemic stroke. Mediators Inflamm. 2014;2014:813045. doi: 10.1155/2014/813045

 

  1. Becker KJ. Inflammation and the silent sequelae of stroke. Neurotherapeutics. 2016;13(4):801-810. doi: 10.1007/s13311-016-0451-5

 

  1. Wen H, Weymann KB, Wood L, Wang QM. Inflammatory signaling in post-stroke fatigue and depression. Eur Neurol. 2018;80(3-4):138-148. doi: 10.1159/000494988

 

  1. O’Connor JC, Satpathy A, Hartman ME, et al. IL-1beta-mediated innate immunity is amplified in the db/db mouse model of type 2 diabetes. J Immunol. 2005;174(8):4991-4997. doi: 10.4049/jimmunol.174.8.4991

 

  1. Pendlebury ST, Rothwell PM, Oxford Vascular Study. Incidence and prevalence of dementia associated with transient ischaemic attack and stroke: Analysis of the population-based Oxford Vascular Study. Lancet Neurol. 2019;18(3):248-258. doi: 10.1016/S1474-4422(18)30442-3

 

  1. Shang Y, Fratiglioni L, Marseglia A, et al. Association of diabetes with stroke and post-stroke dementia: A population-based cohort study. Alzheimers Dement. 2020;16(7):1003-1012. doi: 10.1002/alz.12101

 

  1. Doyle KP, Buckwalter MS. Does B lymphocyte-mediated autoimmunity contribute to post-stroke dementia? Brain Behav Immun. 2017;64:1-8. doi: 10.1016/j.bbi.2016.08.009

 

  1. Belkhelfa M, Beder N, Mouhoub D, et al. The involvement of neuroinflammation and necroptosis in the hippocampus during vascular dementia. J Neuroimmunol. 2018;320:48-57. doi: 10.1016/j.jneuroim.2018.04.004
Conflict of interest
The authors declare that they have no conflicts of interest.
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