Amyloid deposition in intervertebral discs of senescence-accelerated mouse

Shimizu, Katsuji; Ishii, Masaharu; Yamamuro, Takao; Takeshita, S; Hosokawa, Masanori; Takeda, Takeshi

doi:10.1002/art.1780250618

Cited by 23 publications

(3 citation statements)

References 9 publications

(3 reference statements)

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“…Senile Amyloidosis One of the most characteristic pathologic findings in SAM is senile amyloidosis. The organs, except for bone and brain parenchyma, are systemically involved, and the incidence and severity of amyloid deposition increases with advancing age 5–9 . The age dependency of amyloid deposition was recently confirmed biochemically by means of a fluorometric assay method with Thioflavine T which we developed 10,11 …”

Section: Pathologic Phenotypes In Sammentioning

confidence: 92%

Senescence‐Accelerated Mouse (SAM): A Novel Murine Model of Accelerated Senescence

Takeda

Hosokawa

Higuchi

1991

J American Geriatrics Society

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n animal model for accelerated senescence named the Senescence-Accelerated Mouse (SAM) was developed in our laboratory (Department of Senescence Biology, formerly Department of Pathology, Chest Disease Research Institute, Kyoto University) beginning in 1970. In this review, the circumstances related to development of SAM, characteristics of aging, pathologic phenotypes, and genetic background of this model are described. CIRCUMSTANCES OF DEVELOPMENTSeveral pairs of the AKR/J strain of mice were donated by the Jackson Laboratory (Bar Harbor, Maine, USA) to the Department of Pathology, Chest Disease Research Institute, Kyoto University, Japan, in 1968.' While continuing the sister-brother mating to maintain this inbred strain, we became aware of the presence of certain litters in which most of the mice showed a moderate to severe degree of loss of activity, hair loss and lack of glossiness, skin coarseness, periophthalmic lesions,* increased lordokyphosis of the spine, and shortened life span despite the relatively low incidence of thymic lymphoma. We were also aware of inheritance of these phenotypes by the following generations ( Figure 1). As the progenitor of senescence-prone series (P series), five litters with severe exhaustion were selected. Litters in which the aging process was normal were also selected as the progenitors of the senescenceresistant series (R series).' Selecting these progenitors, normal was defined a5 follows: for the preceding three generations, the mean life span had to be more than 16 months and the grading score of senescence less than 2.0 at 8 months of age.3Thereafter, in addition to the routine sister-brother mating, selective breeding was applied based on the data of the grading score of senescence, life span, and pathologic phenotypes. From each of the selected litters with severe exhaustion, five different series designated

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Section: Pathologic Phenotypes In Sammentioning

confidence: 92%

Senescence‐Accelerated Mouse (SAM): A Novel Murine Model of Accelerated Senescence

Takeda

Hosokawa

Higuchi

1991

J American Geriatrics Society

Self Cite

426

243

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“…It has been described in two dogs [19] where it appeared to be immunoreactive like AA-amyloid, whilst in humans articular amyloid deposits are known in haemodialysis patients representing a precipitate of b 2 -microglobulin [20,21], in patients with plasma cell dyscrasia representing AL amyloid [22,23], and at old age being of unknown type [24][25][26][27]. In senescence accelerated mice apoA-II amyloid deposits in intervertebral discs have been described [28][29][30][31].…”

Section: Discussionmentioning

confidence: 99%

Chicken Joint Amyloid Protein is of the AA‐type. I. Characterization of the Amyloid Protein

Landman

Sletten²,

Koch

et al. 1996

Scand J Immunol

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“…SAM-P shows ac celerated changes with many signs of aging, such as a short life span, changes in general behavior, loss of skin glossiness, increased skin coarseness, hair loss, periophthalmic lesion, cataract, increased lordokyphosis of the spine (17), rapid appearance of dysfunc tion in learning and memory (18,19), en hanced systemic amyloidosis (20)(21)(22), loss of bone mass (23), and others. Nomura et al (24) have demonstrated changes in several biochemical parameters related to the degree of senescence in SAM.…”

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confidence: 99%

Effects of Repeated Administrations of Facteur Thymique Sérique (FTS) on Biochemical Changes Related to Aging in Senescence-Accelerated Mouse (SAM)

Zhao

Awaya

Kobayashi

et al. 1990

Japanese Journal of Pharmacology

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Abstract-Superoxide dismutase (SOD) activity, malondialdehyde (MDA) content and monoamine oxidase B (MAO-B) activity were measured in the brain, liver and kidney of a normal aging strain (R/1) and an accelerating aging strain (P/8) senes cence-accelerated mice (SAM) at 9-10 months of age, and the effects of facteur thymique serique (FTS) were examined. The activity of Cu,Zn-SOD in the kidney and MAO-B in the liver was significantly low and high in SAM-P/8 compared to SAM-R/1. FTS enhanced the activity of Mn-SOD and Cu,Zn-SOD in the kidney of SAM-P/8 and Cu,Zn-SOD activity in the brain of both SAM-P/8 and SAM-R/1. It decreased the activity of MAO-B in the liver and the contents of malon dialdehyde (MDA) in the brain and kidney of SAM-P/8. Thus, FTS affects the biochemical factors related to senescence in SAM-P/8, a particular senescent animal model, and may thus possibly be effective as an anti-senescent medicine.Facteur thymique serique (FTS) is a nona peptide which was first isolated from pig serum by and then from the thymus (4). Several studies indicate that FTS exerts an immunobiological effect:

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Amyloid deposition in intervertebral discs of senescence-accelerated mouse

Cited by 23 publications

References 9 publications

Senescence‐Accelerated Mouse (SAM): A Novel Murine Model of Accelerated Senescence

Senescence‐Accelerated Mouse (SAM): A Novel Murine Model of Accelerated Senescence

Chicken Joint Amyloid Protein is of the AA‐type. I. Characterization of the Amyloid Protein

Effects of Repeated Administrations of Facteur Thymique Sérique (FTS) on Biochemical Changes Related to Aging in Senescence-Accelerated Mouse (SAM)

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