β-Amyloid peptide modulates peripheral immune responses and neuroinflammation in rats

Alzheimer’s disease (AD) is characterized by immune system dysregulation, impacting both central and peripheral immune responses. The study aimed to investigate the mechanism behind the neurotoxic effects of β-amyloid (Aβ) peptide in the rat brain including the study of neuroinflammation, neurodegen...

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Main Authors: Adhikary Krishnendu, Mohanty Satyajit, Bandyopadhyay Bidyut, Maiti Rajkumar, Bhattacharya Koushik, Karak Prithviraj
Format: Article
Language:English
Published: De Gruyter 2024-03-01
Series:Biomolecular Concepts
Subjects:
Online Access:https://doi.org/10.1515/bmc-2022-0042
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author Adhikary Krishnendu
Mohanty Satyajit
Bandyopadhyay Bidyut
Maiti Rajkumar
Bhattacharya Koushik
Karak Prithviraj
author_facet Adhikary Krishnendu
Mohanty Satyajit
Bandyopadhyay Bidyut
Maiti Rajkumar
Bhattacharya Koushik
Karak Prithviraj
author_sort Adhikary Krishnendu
collection DOAJ
description Alzheimer’s disease (AD) is characterized by immune system dysregulation, impacting both central and peripheral immune responses. The study aimed to investigate the mechanism behind the neurotoxic effects of β-amyloid (Aβ) peptide in the rat brain including the study of neuroinflammation, neurodegeneration, and alterations in peripheral immune responses (PIR). The neuroinflammation brought on by Aβ1–42 and is unknown to influence PIR. Animal models were prepared, after 28 days, control, sham, and treated rats were anaesthetized and inflammatory markers of hippocampus and serum levels (reactive oxygen species, nitrite, tumor necrosis factor-α, and interleukin-1β), and some markers of PIR (splenic mononuclear cells or MNC, cytotoxicity and phagocytic index of the white blood cells leukocyte adhesion inhibition index or LAI), as well as polymorphonuclear cells of the spleen, were assessed. In addition to changes in peripheral immune responses, the present study found that AD rats had higher blood levels of inflammatory markers. Based on the study, the immune system irregularities observed in AD rats in the peripheral regions might be connected to neuroinflammation, which is facilitated by a compromised blood–brain barrier. Hence, it is viable to propose that the neuroinflammatory condition in rats with Aβ-induced AD could modify immune responses in the peripheral areas with significantly higher levels of inflammatory cytokines markers in the hippocampal tissue in Aβ-injected AD rats.
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spelling doaj.art-1db6af33753f46bead6b58ef577add522024-03-11T10:03:57ZengDe GruyterBiomolecular Concepts1868-503X2024-03-011512415210.1515/bmc-2022-0042β-Amyloid peptide modulates peripheral immune responses and neuroinflammation in ratsAdhikary Krishnendu0Mohanty Satyajit1Bandyopadhyay Bidyut2Maiti Rajkumar3Bhattacharya Koushik4Karak Prithviraj5Department of Interdisciplinary Science, Centurion University of Technology and Management, Odisha 761211, IndiaDepartment of Advanced Pharmacology, Birla Institute of Technology, Mesra, Ranchi, Jharkhand 835215, IndiaDepartment of Biotechnology, Oriental Institute of Science and Technology, Dewandighi, Burdwan, West Bengal 713102, IndiaDepartment of Physiology, Bankura Christian College, Bankura, West Bengal s722101, IndiaSchool of Paramedics and Allied Health Sciences, Centurion University of Technology & Management, Jatni, Bhubaneswar, Odisha 752050, IndiaDepartment of Physiology, Bankura Christian College, Bankura, West Bengal s722101, IndiaAlzheimer’s disease (AD) is characterized by immune system dysregulation, impacting both central and peripheral immune responses. The study aimed to investigate the mechanism behind the neurotoxic effects of β-amyloid (Aβ) peptide in the rat brain including the study of neuroinflammation, neurodegeneration, and alterations in peripheral immune responses (PIR). The neuroinflammation brought on by Aβ1–42 and is unknown to influence PIR. Animal models were prepared, after 28 days, control, sham, and treated rats were anaesthetized and inflammatory markers of hippocampus and serum levels (reactive oxygen species, nitrite, tumor necrosis factor-α, and interleukin-1β), and some markers of PIR (splenic mononuclear cells or MNC, cytotoxicity and phagocytic index of the white blood cells leukocyte adhesion inhibition index or LAI), as well as polymorphonuclear cells of the spleen, were assessed. In addition to changes in peripheral immune responses, the present study found that AD rats had higher blood levels of inflammatory markers. Based on the study, the immune system irregularities observed in AD rats in the peripheral regions might be connected to neuroinflammation, which is facilitated by a compromised blood–brain barrier. Hence, it is viable to propose that the neuroinflammatory condition in rats with Aβ-induced AD could modify immune responses in the peripheral areas with significantly higher levels of inflammatory cytokines markers in the hippocampal tissue in Aβ-injected AD rats.https://doi.org/10.1515/bmc-2022-0042alzheimer’s diseaseneuroinflammationdementiaperipheral immune systemneurodegeneration
spellingShingle Adhikary Krishnendu
Mohanty Satyajit
Bandyopadhyay Bidyut
Maiti Rajkumar
Bhattacharya Koushik
Karak Prithviraj
β-Amyloid peptide modulates peripheral immune responses and neuroinflammation in rats
Biomolecular Concepts
alzheimer’s disease
neuroinflammation
dementia
peripheral immune system
neurodegeneration
title β-Amyloid peptide modulates peripheral immune responses and neuroinflammation in rats
title_full β-Amyloid peptide modulates peripheral immune responses and neuroinflammation in rats
title_fullStr β-Amyloid peptide modulates peripheral immune responses and neuroinflammation in rats
title_full_unstemmed β-Amyloid peptide modulates peripheral immune responses and neuroinflammation in rats
title_short β-Amyloid peptide modulates peripheral immune responses and neuroinflammation in rats
title_sort β amyloid peptide modulates peripheral immune responses and neuroinflammation in rats
topic alzheimer’s disease
neuroinflammation
dementia
peripheral immune system
neurodegeneration
url https://doi.org/10.1515/bmc-2022-0042
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