Localization of atrophy-prone areas in the aging mouse brain: Comparison between the brain atrophy model SAM-P/10 and the normal control SAM-R/1

Shimada, Atsuyoshi; Hosokawa, Masanori; Ohta, Akira; Akiguchi, Ichiro; Takeda, Takeshi

doi:10.1016/0306-4522(94)90290-9

Cited by 56 publications

(26 citation statements)

References 29 publications

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“…In the control SAMR1 mice, there was only a slight macroscopic involutional change in the brain without weight loss, and neither loss of the neocortical large neurons nor shrinkage of the neocortical neurons was evident with aging. The next study [110] was done to analyze age-related changes in brain area size using a computerized morphometric method. A region most vulnerable to agerelated atrophy in the SAMP10 mice was the frontal region of the cerebral cortex, including the prefrontal cortex.…”

Section: Neuropathological Studiesmentioning

confidence: 99%

Senescence-Accelerated Mouse (SAM) with Special References to Neurodegeneration Models, SAMP8 and SAMP10 Mice

Takeda¹

2009

Neurochem Res

215

188

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The SAM strains, a group of related inbred strains consisting of senescence-prone inbred strains (SAMP) and senescence-resistant inbred strains (SAMR), have been successfully developed by selective inbreeding of the AKR/J strain of mice donated by the Jackson laboratory in 1968. The characteristic feature of aging common to the SAMP and SAMR is accelerated senescence and normal aging, respectively. Furthermore, SAMP and SAMR strains of mice manifest various pathobiological phenotypes spontaneously. Among SAMP strains, SAMP8 and SAMP10 mice show age-related behavioral deterioration such as deficits in learning and memory, emotional disorders (reduced anxiety-like behavior and depressive behavior) and altered circadian rhythm associated with certain pathological, biochemical and pharmacological changes. Here, the previous and recent literature on SAM mice are reviewed with an emphasis on SAMP8 and SAMP10 mice. A spontaneous model like SAM with distinct advantages over the gene-modified model is hoped by investigators to be used more widely as a biogerontological resource to explore the etiopathogenesis of accelerated senescence and neurodegenerative disorders.

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Section: Neuropathological Studiesmentioning

confidence: 99%

Senescence-Accelerated Mouse (SAM) with Special References to Neurodegeneration Models, SAMP8 and SAMP10 Mice

Takeda¹

2009

Neurochem Res

215

188

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“…The SAMP 10 strain has the characteristics of a generalized and rapidly developing atrophy of the cerebral hemispheres and it has been used extensively in behavioral research. However, studies have shown that the atrophy is probably pathological, rather than a consequence of accelerated aging, since there are no increases of beta APP mRNA or other relevant protein marker changes during the maturation process (Jeong et al 1997;Shimada et al 1994).…”

Section: Introductionmentioning

confidence: 99%

Cell death in the Purkinje cells of the cerebellum of senescence accelerated mouse (SAMP8)

et al. 2007

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The cerebella of SAMP(8) (accelerated aging mouse) and SAMR(1) controls were analyzed by Western Blotting of tyrosine hydroxylase and choline acetyltransferase, as well as by TUNEL and histological silver staining. Both tyrosine hydroxylase and choline acetyltransferase levels were higher in SAMR(1) than in SAMP(8). There was also an age-related decrease in enzyme levels in SAMP(8), with the reduction of tyrosine hydroxylase being more apparent. Concomitantly, there was an age-related increase of apoptosis in the medial neocerebellum and the vermis as revealed by TUNEL, with changes being significant in the SAMP(8) strain. Histologically, some Purkinje cells appeared to disappear during aging. Taken together, the data suggests that the aging SAMP(8) strain displays differential Purkinje cell death in the medial cerebellum and that some of the dying cells are likely to be catecholaminergic.

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“…Hematoxylinand eosin-stained transverse sections were prepared from four areas of the brains ( Fig. 1): the frontal lobe, the central portion of cerebrum, the mesencephalon, and the medulla-cerebellum (19). Average widths of the meninges were calculated from 15 fields of a stained slide under ϫ100 or ϫ400 magnification to assess the severity of meningitis.…”

Section: Methodsmentioning

confidence: 99%

Combined Treatment with Interleukin-12 and Mebendazole Lessens the Severity of Experimental Eosinophilic Meningitis Caused byAngiostrongylus cantonensisin ICR Mice

Liao

Fan

et al. 2003

Infect Immun

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Angiostrongylus cantonensis is the major cause of eosinophilic meningoencephalitis cases in Taiwan. Mice were orally infected with 35 infective larvae. One group of mice were given a single dose of mebendazole (20 mg/kg of body weight) per os at various times and examined at 14 days postinfection (dpi) for worm recovery rate and pathological studies. A 94 to 97% reduction in worm recovery was observed when medication was given at 4 to 5 dpi. Sections of the brains revealed that untreated infected mice developed typical severe eosinophilic meningoencephalitis. Meninges of these mice were thickened by massive infiltration of eosinophils, whereas only moderate pathological change was observed in the brains of mice that were treated with mebendazole at 4 dpi. Infected mice that received daily injections of 10 ng of interleukin-12 (IL-12) only for various numbers of days also exhibited moderate pathological changes in the brain. Eosinophil infiltration in the brains of these mice was low, and severe mechanical injuries in the parenchyma were observed. Treatment with mebendazole in combination with IL-12, however, resulted in low levels of worm recovery and dramatic lessening of the eosinophilic meningitis. A reverse transcriptase PCR assay of mRNA expression in the brain also revealed that the use of IL-12 had shifted the immune response of the mouse from Th2 type to Th1 type. This study could be used in developing strategies for the treatment of human angiostrongylosis.

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Localization of atrophy-prone areas in the aging mouse brain: Comparison between the brain atrophy model SAM-P/10 and the normal control SAM-R/1

Cited by 56 publications

References 29 publications

Senescence-Accelerated Mouse (SAM) with Special References to Neurodegeneration Models, SAMP8 and SAMP10 Mice

Senescence-Accelerated Mouse (SAM) with Special References to Neurodegeneration Models, SAMP8 and SAMP10 Mice

Cell death in the Purkinje cells of the cerebellum of senescence accelerated mouse (SAMP8)

Combined Treatment with Interleukin-12 and Mebendazole Lessens the Severity of Experimental Eosinophilic Meningitis Caused byAngiostrongylus cantonensisin ICR Mice

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