Protective effects of intracerebroventricular adiponectin against olfactory impairments in an amyloid β1–42 rat model
Abstract Background Alzheimer’s disease (AD) is characterized by cognitive impairment that eventually develops into dementia. Amyloid-beta (Aβ) accumulation is a widely described hallmark in AD, and has been reported to cause olfactory dysfunction, a condition considered an early marker of the disea...
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| Format: | Article |
| Language: | English |
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BMC
2021-03-01
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| Series: | BMC Neuroscience |
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| Online Access: | https://doi.org/10.1186/s12868-021-00620-9 |
| _version_ | 1797699523726802944 |
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| author | Mara A. Guzmán-Ruiz Amor Herrera-González Adriana Jiménez Alan Candelas-Juárez Crystal Quiroga-Lozano Claudia Castillo-Díaz Erika Orta-Salazar Diana Organista-Juárez Sofía Díaz-Cintra Rosalinda Guevara-Guzmán |
| author_facet | Mara A. Guzmán-Ruiz Amor Herrera-González Adriana Jiménez Alan Candelas-Juárez Crystal Quiroga-Lozano Claudia Castillo-Díaz Erika Orta-Salazar Diana Organista-Juárez Sofía Díaz-Cintra Rosalinda Guevara-Guzmán |
| author_sort | Mara A. Guzmán-Ruiz |
| collection | DOAJ |
| description | Abstract Background Alzheimer’s disease (AD) is characterized by cognitive impairment that eventually develops into dementia. Amyloid-beta (Aβ) accumulation is a widely described hallmark in AD, and has been reported to cause olfactory dysfunction, a condition considered an early marker of the disease associated with injuries in the olfactory bulb (OB), the hippocampus (HIPP) and other odor-related cortexes. Adiponectin (APN) is an adipokine with neuroprotective effects. Studies have demonstrated that APN administration decreases Aβ neurotoxicity and Tau hyperphosphorylation in the HIPP, reducing cognitive impairment. However, there are no studies regarding the neuroprotective effects of APN in the olfactory dysfunction observed in the Aβ rat model. The aim of the present study is to determine whether the intracerebroventricular (i.c.v) administration of APN prevents the early olfactory dysfunction in an i.c.v Amyloid-beta1–42 (Aβ1–42) rat model. Hence, we evaluated olfactory function by using a battery of olfactory tests aimed to assess olfactory memory, discrimination and detection in the Aβ rat model treated with APN. In addition, we determined the number of cells expressing the neuronal nuclei (NeuN), as well as the number of microglial cells by using the ionized calcium-binding adapter molecule 1 (Iba-1) marker in the OB and, CA1, CA3, hilus and dentate gyrus (DG) in the HIPP. Finally, we determined Arginase-1 expression in both nuclei through Western blot. Results We observed that the i.c.v injection of Aβ decreased olfactory function, which was prevented by the i.c.v administration of APN. In accordance with the olfactory impairment observed in i.c.v Aβ-treated rats, we observed a decrease in NeuN expressing cells in the glomerular layer of the OB, which was also prevented with the i.c.v APN. Furthermore, we observed an increase of Iba-1 cells in CA1, and DG in the HIPP of the Aβ rats, which was prevented by the APN treatment. Conclusion The present study describes the olfactory impairment of Aβ treated rats and evidences the protective role that APN plays in the brain, by preventing the olfactory impairment induced by Aβ1–42. These results may lead to APN-based pharmacological therapies aimed to ameliorate AD neurotoxic effects. |
| first_indexed | 2024-03-12T04:10:02Z |
| format | Article |
| id | doaj.art-8c57501c11f94be0b5273235a986432f |
| institution | Directory Open Access Journal |
| issn | 1471-2202 |
| language | English |
| last_indexed | 2024-03-12T04:10:02Z |
| publishDate | 2021-03-01 |
| publisher | BMC |
| record_format | Article |
| series | BMC Neuroscience |
| spelling | doaj.art-8c57501c11f94be0b5273235a986432f2023-09-03T11:07:01ZengBMCBMC Neuroscience1471-22022021-03-0122111510.1186/s12868-021-00620-9Protective effects of intracerebroventricular adiponectin against olfactory impairments in an amyloid β1–42 rat modelMara A. Guzmán-Ruiz0Amor Herrera-González1Adriana Jiménez2Alan Candelas-Juárez3Crystal Quiroga-Lozano4Claudia Castillo-Díaz5Erika Orta-Salazar6Diana Organista-Juárez7Sofía Díaz-Cintra8Rosalinda Guevara-Guzmán9Departamento de Fisiología, Facultad de Medicina, Universidad Nacional Autónoma de México (UNAM)Departamento de Fisiología, Facultad de Medicina, Universidad Nacional Autónoma de México (UNAM)Departamento de Fisiología, Facultad de Medicina, Universidad Nacional Autónoma de México (UNAM)Departamento de Fisiología, Facultad de Medicina, Universidad Nacional Autónoma de México (UNAM)Departamento de Fisiología, Facultad de Medicina, Universidad Nacional Autónoma de México (UNAM)Departamento de Fisiología, Facultad de Medicina, Universidad Nacional Autónoma de México (UNAM)Departamento de Neurobiología del desarrollo y neurofisiología, Instituto de Neurobiología, Universidad Nacional Autónoma de México (UNAM)Departamento de Fisiología, Facultad de Medicina, Universidad Nacional Autónoma de México (UNAM)Departamento de Neurobiología del desarrollo y neurofisiología, Instituto de Neurobiología, Universidad Nacional Autónoma de México (UNAM)Departamento de Fisiología, Facultad de Medicina, Universidad Nacional Autónoma de México (UNAM)Abstract Background Alzheimer’s disease (AD) is characterized by cognitive impairment that eventually develops into dementia. Amyloid-beta (Aβ) accumulation is a widely described hallmark in AD, and has been reported to cause olfactory dysfunction, a condition considered an early marker of the disease associated with injuries in the olfactory bulb (OB), the hippocampus (HIPP) and other odor-related cortexes. Adiponectin (APN) is an adipokine with neuroprotective effects. Studies have demonstrated that APN administration decreases Aβ neurotoxicity and Tau hyperphosphorylation in the HIPP, reducing cognitive impairment. However, there are no studies regarding the neuroprotective effects of APN in the olfactory dysfunction observed in the Aβ rat model. The aim of the present study is to determine whether the intracerebroventricular (i.c.v) administration of APN prevents the early olfactory dysfunction in an i.c.v Amyloid-beta1–42 (Aβ1–42) rat model. Hence, we evaluated olfactory function by using a battery of olfactory tests aimed to assess olfactory memory, discrimination and detection in the Aβ rat model treated with APN. In addition, we determined the number of cells expressing the neuronal nuclei (NeuN), as well as the number of microglial cells by using the ionized calcium-binding adapter molecule 1 (Iba-1) marker in the OB and, CA1, CA3, hilus and dentate gyrus (DG) in the HIPP. Finally, we determined Arginase-1 expression in both nuclei through Western blot. Results We observed that the i.c.v injection of Aβ decreased olfactory function, which was prevented by the i.c.v administration of APN. In accordance with the olfactory impairment observed in i.c.v Aβ-treated rats, we observed a decrease in NeuN expressing cells in the glomerular layer of the OB, which was also prevented with the i.c.v APN. Furthermore, we observed an increase of Iba-1 cells in CA1, and DG in the HIPP of the Aβ rats, which was prevented by the APN treatment. Conclusion The present study describes the olfactory impairment of Aβ treated rats and evidences the protective role that APN plays in the brain, by preventing the olfactory impairment induced by Aβ1–42. These results may lead to APN-based pharmacological therapies aimed to ameliorate AD neurotoxic effects.https://doi.org/10.1186/s12868-021-00620-9AdiponectinAmyloid-betaAlzheimer disease modelHippocampusOlfactory bulbOlfactory dysfunction |
| spellingShingle | Mara A. Guzmán-Ruiz Amor Herrera-González Adriana Jiménez Alan Candelas-Juárez Crystal Quiroga-Lozano Claudia Castillo-Díaz Erika Orta-Salazar Diana Organista-Juárez Sofía Díaz-Cintra Rosalinda Guevara-Guzmán Protective effects of intracerebroventricular adiponectin against olfactory impairments in an amyloid β1–42 rat model BMC Neuroscience Adiponectin Amyloid-beta Alzheimer disease model Hippocampus Olfactory bulb Olfactory dysfunction |
| title | Protective effects of intracerebroventricular adiponectin against olfactory impairments in an amyloid β1–42 rat model |
| title_full | Protective effects of intracerebroventricular adiponectin against olfactory impairments in an amyloid β1–42 rat model |
| title_fullStr | Protective effects of intracerebroventricular adiponectin against olfactory impairments in an amyloid β1–42 rat model |
| title_full_unstemmed | Protective effects of intracerebroventricular adiponectin against olfactory impairments in an amyloid β1–42 rat model |
| title_short | Protective effects of intracerebroventricular adiponectin against olfactory impairments in an amyloid β1–42 rat model |
| title_sort | protective effects of intracerebroventricular adiponectin against olfactory impairments in an amyloid β1 42 rat model |
| topic | Adiponectin Amyloid-beta Alzheimer disease model Hippocampus Olfactory bulb Olfactory dysfunction |
| url | https://doi.org/10.1186/s12868-021-00620-9 |
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