Anti-inflammatory and cognitive effects of interferon-β1a (IFNβ1a) in a rat model of Alzheimer's disease 11 Medical and Health Sciences 1109 Neurosciences

Fulvio Plescia, Carla Cannizzaro, Pietro Scaduto, Maria Fatima Massenti, Giovanni Cassata, Natale Belluardo, Giuseppa Mudo', Domenico Nuzzo, Giovanni Cassata, Luca Cicero, Maria Ruscica, Marta Di Carlo, Luigi M. Grimaldi, Domenico Nuzzo, Luca Cicero, Marta Di Carlo, Monica Frinchi

Risultato della ricerca: Article

6 Citazioni (Scopus)

Abstract

Background: Aβ 1-42 peptide abnormal production is associated with the development and maintenance of neuroinflammation and oxidative stress in brains from Alzheimer disease (AD) patients. Suppression of neuroinflammation may then represent a suitable therapeutic target in AD. We evaluated the efficacy of IFNβ1a in attenuating cognitive impairment and inflammation in an animal model of AD. Methods: A rat model of AD was obtained by intra-hippocampal injection of Aβ 1-42 peptide (23 μg/2 μl). After 6 days, 3.6 μg of IFNβ1a was given subcutaneously (s.c.) for 12 days. Using the novel object recognition (NOR) test, we evaluated changes in cognitive function. Measurement of pro-inflammatory or anti-inflammatory cytokines, reactive oxygen species (ROS), and SOD activity levels was performed in the hippocampus. Data were evaluated by one-way ANOVA with Fisher's Protected Least Significant Difference (PLSD) test. Results: We showed that treatment with IFNβ1a was able to reverse memory impairment and to counteract microglia activation and upregulation of pro-inflammatory cytokines (IL-6, IL-1β) in the hippocampus of Aβ 1-42 -injected rats. The anti-inflammatory cytokine IL-10, significantly reduced in the Aβ 1-42 animals, recovered to control levels following IFNβ1a treatment. IFNβ1a also reduced ROS and lipids peroxidation and increased SOD1 protein levels in the hippocampus of Aβ 1-42 -injected rats. Conclusion: This study shows that IFNβ1a is able to reverse the inflammatory and cognitive effects of intra-hippocampal Aβ 1-42 in the rat. Given the role played by inflammation in AD pathogenesis and the established efficacy of IFNβ1a in the treatment of inflammatory diseases of the central nervous system such as multiple sclerosis, its use may be a viable strategy to inhibit the pro-inflammatory cytokine and oxidative stress cascade associated with Aβ deposition in the hippocampus of AD patients.
Lingua originaleEnglish
pagine (da-a)44-59
Numero di pagine16
RivistaDefault journal
Volume16
Stato di pubblicazionePublished - 2019

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)
  • Immunology
  • Neurology
  • Cellular and Molecular Neuroscience

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Anti-inflammatory and cognitive effects of interferon-β1a (IFNβ1a) in a rat model of Alzheimer's disease 11 Medical and Health Sciences 1109 Neurosciences. / Plescia, Fulvio; Cannizzaro, Carla; Scaduto, Pietro; Massenti, Maria Fatima; Cassata, Giovanni; Belluardo, Natale; Mudo', Giuseppa; Nuzzo, Domenico; Cassata, Giovanni; Cicero, Luca; Ruscica, Maria; Di Carlo, Marta; Grimaldi, Luigi M.; Nuzzo, Domenico; Cicero, Luca; Di Carlo, Marta; Frinchi, Monica.

In: Default journal, Vol. 16, 2019, pag. 44-59.

Risultato della ricerca: Article

Plescia, Fulvio ; Cannizzaro, Carla ; Scaduto, Pietro ; Massenti, Maria Fatima ; Cassata, Giovanni ; Belluardo, Natale ; Mudo', Giuseppa ; Nuzzo, Domenico ; Cassata, Giovanni ; Cicero, Luca ; Ruscica, Maria ; Di Carlo, Marta ; Grimaldi, Luigi M. ; Nuzzo, Domenico ; Cicero, Luca ; Di Carlo, Marta ; Frinchi, Monica. / Anti-inflammatory and cognitive effects of interferon-β1a (IFNβ1a) in a rat model of Alzheimer's disease 11 Medical and Health Sciences 1109 Neurosciences. In: Default journal. 2019 ; Vol. 16. pagg. 44-59.
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abstract = "Background: Aβ 1-42 peptide abnormal production is associated with the development and maintenance of neuroinflammation and oxidative stress in brains from Alzheimer disease (AD) patients. Suppression of neuroinflammation may then represent a suitable therapeutic target in AD. We evaluated the efficacy of IFNβ1a in attenuating cognitive impairment and inflammation in an animal model of AD. Methods: A rat model of AD was obtained by intra-hippocampal injection of Aβ 1-42 peptide (23 μg/2 μl). After 6 days, 3.6 μg of IFNβ1a was given subcutaneously (s.c.) for 12 days. Using the novel object recognition (NOR) test, we evaluated changes in cognitive function. Measurement of pro-inflammatory or anti-inflammatory cytokines, reactive oxygen species (ROS), and SOD activity levels was performed in the hippocampus. Data were evaluated by one-way ANOVA with Fisher's Protected Least Significant Difference (PLSD) test. Results: We showed that treatment with IFNβ1a was able to reverse memory impairment and to counteract microglia activation and upregulation of pro-inflammatory cytokines (IL-6, IL-1β) in the hippocampus of Aβ 1-42 -injected rats. The anti-inflammatory cytokine IL-10, significantly reduced in the Aβ 1-42 animals, recovered to control levels following IFNβ1a treatment. IFNβ1a also reduced ROS and lipids peroxidation and increased SOD1 protein levels in the hippocampus of Aβ 1-42 -injected rats. Conclusion: This study shows that IFNβ1a is able to reverse the inflammatory and cognitive effects of intra-hippocampal Aβ 1-42 in the rat. Given the role played by inflammation in AD pathogenesis and the established efficacy of IFNβ1a in the treatment of inflammatory diseases of the central nervous system such as multiple sclerosis, its use may be a viable strategy to inhibit the pro-inflammatory cytokine and oxidative stress cascade associated with Aβ deposition in the hippocampus of AD patients.",
author = "Fulvio Plescia and Carla Cannizzaro and Pietro Scaduto and Massenti, {Maria Fatima} and Giovanni Cassata and Natale Belluardo and Giuseppa Mudo' and Domenico Nuzzo and Giovanni Cassata and Luca Cicero and Maria Ruscica and {Di Carlo}, Marta and Grimaldi, {Luigi M.} and Domenico Nuzzo and Luca Cicero and {Di Carlo}, Marta and Monica Frinchi",
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TY - JOUR

T1 - Anti-inflammatory and cognitive effects of interferon-β1a (IFNβ1a) in a rat model of Alzheimer's disease 11 Medical and Health Sciences 1109 Neurosciences

AU - Plescia, Fulvio

AU - Cannizzaro, Carla

AU - Scaduto, Pietro

AU - Massenti, Maria Fatima

AU - Cassata, Giovanni

AU - Belluardo, Natale

AU - Mudo', Giuseppa

AU - Nuzzo, Domenico

AU - Cassata, Giovanni

AU - Cicero, Luca

AU - Ruscica, Maria

AU - Di Carlo, Marta

AU - Grimaldi, Luigi M.

AU - Nuzzo, Domenico

AU - Cicero, Luca

AU - Di Carlo, Marta

AU - Frinchi, Monica

PY - 2019

Y1 - 2019

N2 - Background: Aβ 1-42 peptide abnormal production is associated with the development and maintenance of neuroinflammation and oxidative stress in brains from Alzheimer disease (AD) patients. Suppression of neuroinflammation may then represent a suitable therapeutic target in AD. We evaluated the efficacy of IFNβ1a in attenuating cognitive impairment and inflammation in an animal model of AD. Methods: A rat model of AD was obtained by intra-hippocampal injection of Aβ 1-42 peptide (23 μg/2 μl). After 6 days, 3.6 μg of IFNβ1a was given subcutaneously (s.c.) for 12 days. Using the novel object recognition (NOR) test, we evaluated changes in cognitive function. Measurement of pro-inflammatory or anti-inflammatory cytokines, reactive oxygen species (ROS), and SOD activity levels was performed in the hippocampus. Data were evaluated by one-way ANOVA with Fisher's Protected Least Significant Difference (PLSD) test. Results: We showed that treatment with IFNβ1a was able to reverse memory impairment and to counteract microglia activation and upregulation of pro-inflammatory cytokines (IL-6, IL-1β) in the hippocampus of Aβ 1-42 -injected rats. The anti-inflammatory cytokine IL-10, significantly reduced in the Aβ 1-42 animals, recovered to control levels following IFNβ1a treatment. IFNβ1a also reduced ROS and lipids peroxidation and increased SOD1 protein levels in the hippocampus of Aβ 1-42 -injected rats. Conclusion: This study shows that IFNβ1a is able to reverse the inflammatory and cognitive effects of intra-hippocampal Aβ 1-42 in the rat. Given the role played by inflammation in AD pathogenesis and the established efficacy of IFNβ1a in the treatment of inflammatory diseases of the central nervous system such as multiple sclerosis, its use may be a viable strategy to inhibit the pro-inflammatory cytokine and oxidative stress cascade associated with Aβ deposition in the hippocampus of AD patients.

AB - Background: Aβ 1-42 peptide abnormal production is associated with the development and maintenance of neuroinflammation and oxidative stress in brains from Alzheimer disease (AD) patients. Suppression of neuroinflammation may then represent a suitable therapeutic target in AD. We evaluated the efficacy of IFNβ1a in attenuating cognitive impairment and inflammation in an animal model of AD. Methods: A rat model of AD was obtained by intra-hippocampal injection of Aβ 1-42 peptide (23 μg/2 μl). After 6 days, 3.6 μg of IFNβ1a was given subcutaneously (s.c.) for 12 days. Using the novel object recognition (NOR) test, we evaluated changes in cognitive function. Measurement of pro-inflammatory or anti-inflammatory cytokines, reactive oxygen species (ROS), and SOD activity levels was performed in the hippocampus. Data were evaluated by one-way ANOVA with Fisher's Protected Least Significant Difference (PLSD) test. Results: We showed that treatment with IFNβ1a was able to reverse memory impairment and to counteract microglia activation and upregulation of pro-inflammatory cytokines (IL-6, IL-1β) in the hippocampus of Aβ 1-42 -injected rats. The anti-inflammatory cytokine IL-10, significantly reduced in the Aβ 1-42 animals, recovered to control levels following IFNβ1a treatment. IFNβ1a also reduced ROS and lipids peroxidation and increased SOD1 protein levels in the hippocampus of Aβ 1-42 -injected rats. Conclusion: This study shows that IFNβ1a is able to reverse the inflammatory and cognitive effects of intra-hippocampal Aβ 1-42 in the rat. Given the role played by inflammation in AD pathogenesis and the established efficacy of IFNβ1a in the treatment of inflammatory diseases of the central nervous system such as multiple sclerosis, its use may be a viable strategy to inhibit the pro-inflammatory cytokine and oxidative stress cascade associated with Aβ deposition in the hippocampus of AD patients.

UR - http://hdl.handle.net/10447/348022

UR - http://www.jneuroinflammation.com/home/

M3 - Article

VL - 16

SP - 44

EP - 59

JO - Default journal

JF - Default journal

ER -