Systemic inflammation in Aβ 1-40 -induced Alzheimer's disease model: New translational opportunities.

Autor: Nefodova A; Educational and Scientific Centre 'Institute of Biology and Medicine', Taras Shevchenko National University of Kyiv, 2, Hlushkov Avenue, Kyiv 03022, Ukraine., Rudyk M; Educational and Scientific Centre 'Institute of Biology and Medicine', Taras Shevchenko National University of Kyiv, 2, Hlushkov Avenue, Kyiv 03022, Ukraine. Electronic address: 3rudyk_marie@knu.ua., Dovhyi R; Educational and Scientific Centre 'Institute of Biology and Medicine', Taras Shevchenko National University of Kyiv, 2, Hlushkov Avenue, Kyiv 03022, Ukraine., Dovbynchuk T; Educational and Scientific Centre 'Institute of Biology and Medicine', Taras Shevchenko National University of Kyiv, 2, Hlushkov Avenue, Kyiv 03022, Ukraine., Dzubenko N; Educational and Scientific Institute of High Technologies, Taras Shevchenko University of Kyiv, 4g, Hlushkov Avenue, Kyiv 03022, Ukraine., Tolstanova G; Educational and Scientific Institute of High Technologies, Taras Shevchenko University of Kyiv, 4g, Hlushkov Avenue, Kyiv 03022, Ukraine., Skivka L; Educational and Scientific Centre 'Institute of Biology and Medicine', Taras Shevchenko National University of Kyiv, 2, Hlushkov Avenue, Kyiv 03022, Ukraine.
Jazyk: angličtina
Zdroj: Brain research [Brain Res] 2024 Aug 15; Vol. 1837, pp. 148960. Date of Electronic Publication: 2024 Apr 26.
DOI: 10.1016/j.brainres.2024.148960
Abstrakt: Alzheimer disease (AD) is the most frequent cause of dementia, and the most common neurodegenerative disease, which is characterized by memory impairment, neuronal death, and synaptic loss in the hippocampus. Sporadic late-onset AD, which accounts for over 95 % of disease cases, is a multifactorial pathology with complex etiology and pathogenesis. Nowadays, neuroinflammation is considered the third most important component of AD pathogenesis in addition to amyloid peptide generation and deposition. Neuroinflammation is associated with the impairment of blood-brain barrier and leakage of inflammatory mediators into the periphery with developing systemic inflammatory responses. Systemic inflammation is currently considered one of the therapeutic targets for AD treatment, that necessitates in-depth study of this phenomenon in appropriate non-transgenic animal models. This study was aimed to explore systemic inflammatory manifestations in rats with Aβ 1-40 -induced AD. The impairment of spatial memory and cognitive flexibility in Aβ 1-40 -lesioned rats was accompanied by pronounced systemic inflammation, which was confirmed by commonly accepted biomarkers: increased hematological indices of systemic inflammation (NLR, dNLR, LMR, PLR and SII), signs of anemia of inflammation or chronic diseases, and pro-inflammatory polarized activation of circulating phagocytes. In addition, markers of systemic inflammation strongly correlated with disorders of remote cognitive flexibility in Aβ 1-40 -lesioned rats. These results indicate, that Aβ 1-40 -induced AD model permits the investigation of specific element of the disease - systemic inflammation in addition to well reproduced neuroinflammation and impairment of spatial memory and cognitive flexibility. It increases translational value of this well-known model.
Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
(Copyright © 2024 Elsevier B.V. All rights reserved.)
Databáze: MEDLINE
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