Involvement of pro-inflammatory cytokines and microglia in an age-associated neurodegeneration model, the SAMP10 mouse

Naoko Kumagai; Yoichi Chiba; Masamichi Hosono; Masato Fujii; Noriko Kawamura; Hiromi Keino; Keisuke Yoshikawa; Sanae Ishii; Yuko Saitoh; Mamoru Satoh; Atsuyoshi Shimada; Masanori Hosokawa

doi:10.1016/j.brainres.2007.09.021

Involvement of pro-inflammatory cytokines and microglia in an age-associated neurodegeneration model, the SAMP10 mouse

Naoko Kumagai, Yoichi Chiba, Masamichi Hosono, Masato Fujii, Noriko Kawamura, Hiromi Keino, Keisuke Yoshikawa, Sanae Ishii, Yuko Saitoh, Mamoru Satoh, Atsuyoshi Shimada, Masanori Hosokawa

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Abstract

The SAMP10 mouse strain is a model of brain aging in which senescence is characterized by cerebral atrophy and neurodegeneration phenotypes. To investigate the role of neuroinflammation in the age-associated neurodegeneration of SAMP10 mice, we assessed the expression of several cytokines and chemokines in the atrophy-prone brain region of SAMP10, and control, SAMR1 mice, which show a normal aging process. We also studied morphological changes in microglia with advancing age in atrophied regions. The expression of IL-1β and IFN-γ mRNA was about 2-fold greater in SAMP10 mice as compared to SAMR1 mice throughout their life span. The expression of IL-6 mRNA was 2.0-fold greater in SAMP10 mice as compared to SAMR1 mice at 14 months of age, although there was no difference at 3 months of age. Fourteen-month-old mice had a 2.1-fold greater expression of TNF-α mRNA than 3-month-old mice in both strains. The expression of MCP-1 mRNA was greater in SAMP10 mice than SAMR1 mice, and tended to increase with advancing age. Activated microglia were rarely observed in both strains at 3 months of age. At 14 months of age, however, SAMP10 mice had a 5.6-fold greater number of activated microglia than SAMR1 mice. The aforementioned results suggest the presence of a higher pro-inflammatory status in the atrophy-prone brain region of SAMP10 mice as compared to SAMR1 mice. Neuroinflammation is a possible mechanism of age-associated neurodegeneration in SAMP10 mice.

Original language	English (US)
Pages (from-to)	75-85
Number of pages	11
Journal	Brain research
Volume	1185
Issue number	1
DOIs	https://doi.org/10.1016/j.brainres.2007.09.021
State	Published - Dec 14 2007

All Science Journal Classification (ASJC) codes

General Neuroscience
Molecular Biology
Clinical Neurology
Developmental Biology

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10.1016/j.brainres.2007.09.021

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@article{94221b6005bb468e871d18938a131853,

title = "Involvement of pro-inflammatory cytokines and microglia in an age-associated neurodegeneration model, the SAMP10 mouse",

abstract = "The SAMP10 mouse strain is a model of brain aging in which senescence is characterized by cerebral atrophy and neurodegeneration phenotypes. To investigate the role of neuroinflammation in the age-associated neurodegeneration of SAMP10 mice, we assessed the expression of several cytokines and chemokines in the atrophy-prone brain region of SAMP10, and control, SAMR1 mice, which show a normal aging process. We also studied morphological changes in microglia with advancing age in atrophied regions. The expression of IL-1β and IFN-γ mRNA was about 2-fold greater in SAMP10 mice as compared to SAMR1 mice throughout their life span. The expression of IL-6 mRNA was 2.0-fold greater in SAMP10 mice as compared to SAMR1 mice at 14 months of age, although there was no difference at 3 months of age. Fourteen-month-old mice had a 2.1-fold greater expression of TNF-α mRNA than 3-month-old mice in both strains. The expression of MCP-1 mRNA was greater in SAMP10 mice than SAMR1 mice, and tended to increase with advancing age. Activated microglia were rarely observed in both strains at 3 months of age. At 14 months of age, however, SAMP10 mice had a 5.6-fold greater number of activated microglia than SAMR1 mice. The aforementioned results suggest the presence of a higher pro-inflammatory status in the atrophy-prone brain region of SAMP10 mice as compared to SAMR1 mice. Neuroinflammation is a possible mechanism of age-associated neurodegeneration in SAMP10 mice.",

author = "Naoko Kumagai and Yoichi Chiba and Masamichi Hosono and Masato Fujii and Noriko Kawamura and Hiromi Keino and Keisuke Yoshikawa and Sanae Ishii and Yuko Saitoh and Mamoru Satoh and Atsuyoshi Shimada and Masanori Hosokawa",

note = "Funding Information: We thank Dr. N. Wakamatsu from the Department of Genetics, Institute for Developmental Research, Aichi Human Service Center, and Dr. Y. Nishimura and Prof. T. Otsuki from the Department of Hygiene, Kawasaki Medical School. Gratitude is also extended to K. Gotoh, T. Kumata, R. Ikeda, Y. Shimizu, and S. Narumi from the Laboratory of Immunobiology, Niigata University. This work was supported by the Sasakawa Scientific Research Grant from The Japan Science Society (No.18-130).",

year = "2007",

month = dec,

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doi = "10.1016/j.brainres.2007.09.021",

language = "English (US)",

volume = "1185",

pages = "75--85",

journal = "Brain research",

issn = "0006-8993",

publisher = "Elsevier B.V.",

number = "1",

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TY - JOUR

T1 - Involvement of pro-inflammatory cytokines and microglia in an age-associated neurodegeneration model, the SAMP10 mouse

AU - Kumagai, Naoko

AU - Chiba, Yoichi

AU - Hosono, Masamichi

AU - Fujii, Masato

AU - Kawamura, Noriko

AU - Keino, Hiromi

AU - Yoshikawa, Keisuke

AU - Ishii, Sanae

AU - Saitoh, Yuko

AU - Satoh, Mamoru

AU - Shimada, Atsuyoshi

AU - Hosokawa, Masanori

N1 - Funding Information: We thank Dr. N. Wakamatsu from the Department of Genetics, Institute for Developmental Research, Aichi Human Service Center, and Dr. Y. Nishimura and Prof. T. Otsuki from the Department of Hygiene, Kawasaki Medical School. Gratitude is also extended to K. Gotoh, T. Kumata, R. Ikeda, Y. Shimizu, and S. Narumi from the Laboratory of Immunobiology, Niigata University. This work was supported by the Sasakawa Scientific Research Grant from The Japan Science Society (No.18-130).

PY - 2007/12/14

Y1 - 2007/12/14

N2 - The SAMP10 mouse strain is a model of brain aging in which senescence is characterized by cerebral atrophy and neurodegeneration phenotypes. To investigate the role of neuroinflammation in the age-associated neurodegeneration of SAMP10 mice, we assessed the expression of several cytokines and chemokines in the atrophy-prone brain region of SAMP10, and control, SAMR1 mice, which show a normal aging process. We also studied morphological changes in microglia with advancing age in atrophied regions. The expression of IL-1β and IFN-γ mRNA was about 2-fold greater in SAMP10 mice as compared to SAMR1 mice throughout their life span. The expression of IL-6 mRNA was 2.0-fold greater in SAMP10 mice as compared to SAMR1 mice at 14 months of age, although there was no difference at 3 months of age. Fourteen-month-old mice had a 2.1-fold greater expression of TNF-α mRNA than 3-month-old mice in both strains. The expression of MCP-1 mRNA was greater in SAMP10 mice than SAMR1 mice, and tended to increase with advancing age. Activated microglia were rarely observed in both strains at 3 months of age. At 14 months of age, however, SAMP10 mice had a 5.6-fold greater number of activated microglia than SAMR1 mice. The aforementioned results suggest the presence of a higher pro-inflammatory status in the atrophy-prone brain region of SAMP10 mice as compared to SAMR1 mice. Neuroinflammation is a possible mechanism of age-associated neurodegeneration in SAMP10 mice.

AB - The SAMP10 mouse strain is a model of brain aging in which senescence is characterized by cerebral atrophy and neurodegeneration phenotypes. To investigate the role of neuroinflammation in the age-associated neurodegeneration of SAMP10 mice, we assessed the expression of several cytokines and chemokines in the atrophy-prone brain region of SAMP10, and control, SAMR1 mice, which show a normal aging process. We also studied morphological changes in microglia with advancing age in atrophied regions. The expression of IL-1β and IFN-γ mRNA was about 2-fold greater in SAMP10 mice as compared to SAMR1 mice throughout their life span. The expression of IL-6 mRNA was 2.0-fold greater in SAMP10 mice as compared to SAMR1 mice at 14 months of age, although there was no difference at 3 months of age. Fourteen-month-old mice had a 2.1-fold greater expression of TNF-α mRNA than 3-month-old mice in both strains. The expression of MCP-1 mRNA was greater in SAMP10 mice than SAMR1 mice, and tended to increase with advancing age. Activated microglia were rarely observed in both strains at 3 months of age. At 14 months of age, however, SAMP10 mice had a 5.6-fold greater number of activated microglia than SAMR1 mice. The aforementioned results suggest the presence of a higher pro-inflammatory status in the atrophy-prone brain region of SAMP10 mice as compared to SAMR1 mice. Neuroinflammation is a possible mechanism of age-associated neurodegeneration in SAMP10 mice.

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JF - Brain research

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Involvement of pro-inflammatory cytokines and microglia in an age-associated neurodegeneration model, the SAMP10 mouse

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