The relationship of amyloidogenesis and taupathy with clinical outcomes of cerebral ischemia. Experimental research

Original article

УДК 616-003.821
DOI: 10.57034/2618723X-2023-02-02

D.I. Pozdnyakov*,
Associate professor of the Department of Pharmacology with a course of clinical pharmacology,

Pyatigorsk Medical and Pharmaceutical Institute — branch of the Volga State Medical University,
357532, Russia Stavropol Territory, Pyatigorsk, Kalinin ave., 11.

* E-mail: [email protected]

Keywords: brain ischemia beta-amyloid tau protein cognitive deficit neurological deficit sensorimotor deficit


The study was performed without external funding.

For citation:

Pozdnyakov D. I. The relationship of amyloidogenesis and taupathy with clinical outcomes of cerebral ischemia. Experimental research. Laboratory Animals for Science. 2023; 2.


Currently, it has been established that increased formation of β-amyloid and tau protein play a significant role in the pathogenesis of cerebral ischemia. At the same time, these molecules can act as prognostic markers of the severity of cerebral ischemia. The aim of the study. To evaluate the peculiarities of changes in the concentration of β-amyloid and tau protein in blood serum and cerebrospinal fluid in rats with experimental subtotal cerebral ischemia, as well as to establish their relationship with the severity of post-ischemic clinical changes. Materials and methods. Subtotal cerebral ischemia was modeled by simultaneous occlusion of common carotid arteries in Wistar rats. The study assessed changes in neurological, sensorimotor and cognitive deficits. The content of β-amyloid and tau protein was assessed in blood serum and cerebrospinal fluid on the 1st, 3rd, 5th and 7th days of ischemia. During the analysis, species-specific kits for solid-phase enzyme immunoassay were used. Results. It was found that in animals with subtotal cerebral ischemia, as the duration of the ischemic period increases from day 1 to day 7, the concentration of β-amyloid and tau protein in both blood serum and cerebrospinal fluid progressively increases. It is worth noting that these changes strongly correlated with changes in the clinical manifestations of cerebral ischemia — neurological, sensorimotor and cognitive deficits.

Conflict of interest

The authors declare no conflict of interest.

  1. Директива 2010/63/EU Европейского парламента и Совета Европейского союза по охране животных, используемых в научных целях / пер. с англ. Под ред. М.С. Красильщиковой, И.В. Белозерцевой. Санкт-Петербург, 2012. 48 с. [Direktiva 2010/63/EU Yevropeyskogo Parlamenta i Soveta Yevropeyskogo Soyuza po okhrane zhivotnykh, ispol’zuyemykh v nauchnykh tselyakh / transl. from English. Ed. M.S. Krasilshchikova, I.V. Belozertseva. St. Petersburg, 2012. 48 p. (In Russ.)].


  1. Xu M., Feng T., Liu B. et. al. Engineered exosomes: desirable target-tracking charac­teristics for cerebrovascular and neurodegenerative disease therapies // Theranostics. 2021. Vol. 11. N. 18. Р. 8926–8944.
  2. Rabinstein A.A. Update on Treatment of Acute Ischemic Stroke // Continuum (Minneap Minn). 2020. Vol. 26. N. 2. Р. 268–286.
  3. Zhao Y., Zhang X., Chen X., Wei Y. Neuronal injuries in cerebral infarction and ischemic stroke: From mecha­nisms to treatment (Review) // Int. J. Mol. Med. 2022. Vol. 49. N. 2. Р. 15.
  4. Pluta R., Bogucka-Kocka A., Ułamek-Kozioł M. Ischemic tau protein gene induction as an additional key factor driving development of Alzheimer’s phenotype chan­ges in CA1 area of hippocampus in an ischemic model of Alzheimer’s disease // Pharmacol Rep. 2018. Vol. 70. N. 5. Р. 881–884.
  5. Wiatrak B., Piasny J., Kuźniarski A., Gąsiorowski K. Interactions of Amyloid-β with Membrane Proteins // Int. J. Mol. Sci. 2021. Vol. 22. N. 11. Р. 6075.
  6. Liang S.Y., Wang Z.T., Tan L., Yu J.T. Tau Toxicity in Neurodegeneration // Mol. Neurobiol. 2022. Vol. 59. N. 6. Р. 3617–3634.
  7. Esteves-Villanueva J.O., Trzeciakiewicz H., Martic S. A protein-based electrochemical biosensor for detection of tau protein, a neurodegenerative disease biomarker // Analyst. 2014. Vol. 139. N. 11. Р. 2823–2831.
  8. Yakupova E.I., Bobyleva L.G., Vikhlyantsev I.M., Bobylev A.G. Congo Red and amyloids: history and relationship // Biosci Rep. 2019. Vol. 9. N. 1. Р. 20181415.
  9. Katayama Y, Sugimoto S, Inamura K. Susceptibility to ischemic insult in hypertensive rats: correlation between degree of ischemia and hypertension // Jpn. Circ. J. 1986. Vol. 50. N. 3. Р. 258–264.
  10. Sheila M. Fleming, Osunde R. Ekhator, Valentins Ghisays. Assessment of Sensorimotor Function in Mouse Models of Parkinson’s Disease // J. Vis. Exp. 2013. Vol. 76. Р. 50303.
  11. Amani M., Zolghadrnasab M., Salari A.A. NMDA receptor in the hippocampus alters neurobehavioral phenotypes through inflammatory cytokines in rats with sporadic Alzheimer-like disease // Physiol Behav. 2019. Vol. 202. P. 52–61.
  12. Akoglu H. User’s guide to correlation coefficients // Turk. J. Emerg. Med. 2018. Vol. 18. N. 3. P. 91–93.
  13. Pluta R., Januszewski S., Jabłoński M. Acetylated Tau Protein: A New Piece in the Puzzle between Brain Ische­mia and Alzheimer’s Disease // Int. J. Mol. Sci. 2022. Vol. 23. N. 16. Р. 9174.
  14. Pluta R., Jabłoński M., Czuczwar S.J. Postischemic dementia with Alzheimer phenotype: selectively vulnerable versus resistant areas of the brain and neurodegene­ration versus β-amyloid peptide // Folia Neuropathol. 2012. Vol. 50. N. 2. Р. 101–109.
  15. Pluta R, Januszewski S, Czuczwar SJ. Brain Ischemia as a Prelude to Alzheimer’s Disease // Front Aging Neuro­sci. 2021. Vol. 13. Р. 636653.
  16. Pluta R., Kiś J., Januszewski S., Jabłoński M., Czuczwar S.J. Cross-Talk between Amyloid, Tau Protein and Free Radicals in Post-Ischemic Brain Neurodege­neration in the Form of Alzheimer’s Disease Proteino­pathy // Antioxidants (Basel). 2022. Vol. 11. N. 1. Р. 146.
  17. De Vos A., Bjerke M., Brouns R. et. al. Neurogranin and tau in cerebrospinal fluid and plasma of patients with acute ischemic stroke // BMC Neurol. 2017. Vol. 17. N. 1. Р. 170.
  18. Lasek-Bal A., Jedrzejowska-Szypulka H., Rozycka J. et al. The presence of Tau protein in blood as a potential prognostic factor in stroke patients // J. Physiol. Pharmacol. 2016. Vol. 67. N. 5. Р. 691–696.

Received: 2023-03-18
Reviewed: 2023-05-12
Accepted for publication: 2023-05-23

You may be interested