Neuroinflammatory, Neurodegenerative and Structural Brain Biomarkers of the Main Types of Post-Stroke Cognitive Impairment in Acute Period of Ischemic Stroke

Cover Page


Cite item

Full Text

Abstract

Background. Post-stroke cognitive impairment is a clinically heterogeneous condition, some types of which cannot be fully differentiated neuropsychologically that necessitates the active search for biomarkers. Aims: analyze parameters of neuroinflammation and neurodegeneration in combination with neuroimaging markers in patients with different types of post-stroke cognitive impairment in acute ischemic stroke.

Materials and methods. In 72 patients we performed the assessment of cognitive status and distinguished 3 types: normal cognition, dysexecutive, and mixed cognitive impairment. In each group we determined the concentration of cytokines (IL-1β, IL-6, TNFα, IL-10) in liquor and serum, β-amyloid 1−40 in liquor and a number of MRI morphometric parameters and fractional anisotropy.

Results. In all groups of patients we detected higher level of
IL-10 in serum compared with the control. Patients with dysexecutive cognitive impairment had higher concentration of IL-1β, IL-10 in liquor, IL-6 level in serum, lower fractional anisotropy of ipsilateral thalamus compared with patients with normal cognition and largest size of infarct. Patients with dysexecutive and mixed cognitive impairment had the higher area of leukoareosis and ventricular volume, reduced fractional anisotropy of contralateral cingulum compared with patients with normal cognition. Patients with mixed cognitive impairment characterized by lower fractional anisotropy of contralateral fronto-occipital fasciculus compared with patients with dysexecutive cognitive deficit.

Conclusions. Serum and cerebrospinal fluid concentrations of cytokines studied in combination with MRI parameters particularly fractional anisotropy seems to be informative biomarkers of pathogenic types of PSCI.

About the authors

A. A. Kulesh

Perm State Medical University, Perm, Russian Federation

Author for correspondence.
Email: aleksey.kulesh@gmail.com

кандидат медицинских наук, доцент кафедры неврологии ФДПО Пермского государственного медицинского университета имени академика Е.А. Вагнера Адрес: 614990, Пермь, ул. Петропавловская, д. 26, тел.: +7 (982) 498-33-51

Russian Federation

V. E. Drobakha

Perm State Medical University, Perm, Russian Federation

Email: drobakha.v@gmail.com

ассистент кафедры лучевой диагностики Пермского государственного медицинского университета имени академика Е.А. Вагнера Адрес: 614990, Пермь, ул. Петропавловская, д. 26

Russian Federation

I. V. Nekrasova

Institute of Ecology and Genetics of Microorganisms, Ural Branch of the Russian Academy of Sciences, Perm, Russian Federation

Email: nirina5@mail.ru

кандидат медицинских наук, научный сотрудник лаборатории иммунорегуляции Института экологии и генетики микроорганизмов Уральского отделения РАН Адрес: 614081, Пермь, ул. Голева, д. 13

Russian Federation

E. M. Kuklina

Institute of Ecology and Genetics of Microorganisms, Ural Branch of the Russian Academy of Sciences, Perm, Russian Federation

Email: ibis_07@mail.ru

доктор биологических наук, ведущий научный сотрудник лаборатории иммунорегуляции Института экологии и генетики микроорганизмов Уральского отделения РАН Адрес: 614081, Пермь, ул. Голева, д. 13

V. V. Shestakov

Perm State Medical University, Perm, Russian Federation

Email: shvnerv@mail.ru

доктор медицинских наук, профессор, заведующий кафедрой неврологии ФДПО Пермского государственного медицинского университета имени академика Е.А. Вагнера Адрес: 614990, Пермь, ул. Петропавловская, д. 26

References

  1. Strong K, Mathers C, Bonita R. Preventing stroke: saving lives around the world. Lancet Neurol. 2007;6(2):182–187. doi: 10.1016/S1474-4422(07)70031-5.
  2. Merino JG. Dementia after stroke: high incidence and intriguing associations. Stroke. 2002;33(9):2261–2262.
  3. Sun JH, Tan L, Yu JT. Post-stroke cognitive impairment: epidemiology, mechanisms and management. Ann Transl Med. 2014;2(8):80. doi: 10.3978/j.issn.2305-5839.2014.08.05.
  4. Whitehead SN, Hachinski VC, Cechetto DF. Interaction between a rat model of cerebral ischemia and beta-amyloid toxicity: inflammatory responses. Stroke. 2005;36(1):107–112. doi: 10.1161/01.STR.0000149627.30763.f9.
  5. Sperling R, Johnson K. Biomarkers of Alzheimer disease: current and future applications to diagnostic criteria. Continuum (Minneap Minn). 2013;19(2 Dementia):325–338. doi: 10.1212/01. CON.0000429181.60095.99.
  6. Tobin MK, Bonds JA, Minshall RD, et al. Neurogenesis and inflammation after ischemic stroke: what is known and where we go from here. J Cereb Blood Flow Metab. 2014;34(10):1573–1584. doi: 10.1038/jcbfm.2014.130.
  7. Aktas O, Ullrich O, Infante-Duarte C, et al. Neuronal damage in brain inflammation. Arch Neurol. 2007;64(2):185–189. doi: 10.1001/archneur.64.2.185.
  8. Janardhan V, Qureshi AI. Mechanisms of ischemic brain injury. Curr Cardiol Rep. 2004;6(2):117– 123. doi: 10.1007/s11886-004- 0009-8.
  9. Iadecola C, Anrather J. The immunology of stroke: from mechanisms to translation. Nat Med. 2011;17(7):796–808. doi: 10.1038/nm.2399.
  10. Doyle KP, Quach LN, Sole M, et al. B-lymphocyte-mediated delayed cognitive impairment following stroke. J Neurosci. 2015;35(5):2133–2145. doi: 10.1523/JNEUROSCI.4098-14.2015.
  11. Silva B, Sousa L, Miranda A, et al. Memory deficit associated with increased brain proinflammatory cytokine levels and neurodegeneration in acute ischemic stroke. Arq Neuropsiquiatr. 2015;73(8):655–659. doi: 10.1590/0004-282X20150083.
  12. Thiel A, Radlinska BA, Paquette C, et al. The temporal dynamics of poststroke neuroinflammation: a longitudinal diffusion tensor imaging-guided PET study with 11C-PK11195 in acute subcortical stroke. J Nucl Med. 2010;51(9):1404–1412. doi: 10.2967/jnumed.110.076612.
  13. Radlinska B, Ghinani S, Leppert IR, et al. Diffusion tensor imaging, permanent pyramidal tract damage, and outcome in subcortical stroke. Neurology. 2010;75(12):1048–1054. doi: 10.1212/ WNL.0b013e3181f39aa0.
  14. Radlinska BA, Blunk Y, Leppert IR, et al. Changes in callosal motor fiber integrity after subcortical stroke of the pyramidal tract. J Cereb Blood Flow Metab. 2012;32(8):1515–1524. doi: 10.1038/ jcbfm.2012.37.
  15. Кулеш А.А., Шестаков В.В. Постинсультные когнитивные нарушения и возможности терапии препаратом целлекс //Журнал неврологии и психиатрии им. С.С. Корсакова. — 2016. — Т.116. — №5. — С. 38–42. [Kulesh AA, Shestakov VV. Poststroke cognitive impairment and the possibility of treatment with cellex. Zh Nevrol Psikhiatr Im S S Korsakova. 2016;116(5):8– 42. (In Russ).]
  16. Kliper E, Bashat DB, Bornstein NM, et al. Cognitive decline after stroke: relation to inflammatory biomarkers and hippocampal volume. Stroke. 2013;44(5):1433–1435. doi: 10.1161/ STROKEAHA.111.000536.
  17. Yirmiya R, Goshen I. Immune modulation of learning, memory, neural plasticity and neurogenesis. Brain Behav Immun. 2011;25(2):181–213. doi: 10.1016/j.bbi.2010.10.015.
  18. Goshen I, Kreisel T, Ounallah-Saad H, et al. A dual role for interleukin-1 in hippocampal- dependent memory processes. Psychoneuroendocrinology. 2007;32(8–10):1106–1115. doi: 10.1016/j.psyneuen.2007.09.004.
  19. Mooijaart SP, Sattar N, Trompet S, et al. Circulating interleukin-6 concentration and cognitive decline in old age: the PROSPER study. J Intern Med. 2013;274(1):77–85. doi: 10.1111/joim.12052.
  20. Singh-Manoux A, Dugravot A, Brunner E, et al. Interleukin-6 and C-reactive protein as predictors of cognitive decline in late midlife. Neurology. 2014;83(6):486–493. doi: 10.1212/ WNL.0000000000000665.
  21. Liu W, Wong A, Au L, et al. Influence of Amyloid-beta on Cognitive Decline After Stroke/Transient Ischemic Attack: Three-Year Longitudinal Study. Stroke. 2015;46(11):3074–3080. doi: 10.1161/STROKEAHA.115.010449.
  22. Dacosta-Aguayo R, Grana M, Fernandez-Andujar M, et al. Structural integrity of the contralesional hemisphere predicts cognitive impairment in ischemic stroke at three months. PLoS One. 2014;9(1):e86119. doi: 10.1371/journal.pone.0086119.
  23. Fernandez-Andujar M, Soriano-Raya JJ, Miralbell J, et al. Thalamic diffusion differences related to cognitive function in white matter lesions. Neurobiol Aging. 2014;35(5):1103–1110. doi: 10.1016/j.neurobiolaging.2013.10.087.
  24. Duering M, Gesierich B, Seiler S, et al. Strategic white matter tracts for processing speed deficits in age-related sm all vessel disease. Neurology. 2014;82(22):1946–1950. doi: 10.1212/ WNL.0000000000000475.
  25. Palm WM, Saczynski JS, van der Grond J, et al. Ventricular dilation: association with gait and cognition. Ann Neurol. 2009;66(4):485–493. doi: 10.1002/ana.21739.
  26. Dong C, Nabizadeh N, Caunca M, et al. Cognitive correlates of white matter lesion load and brain atrophy: the Northern Manhattan Study. Neurology. 2015;85(5):441–449. doi: 10.1212/WNL.0000000000001716.

Supplementary files

Supplementary Files
Action
1. JATS XML
Download

Copyright (c) 2016 "Paediatrician" Publishers LLC



This website uses cookies

You consent to our cookies if you continue to use our website.

About Cookies