Apical vulnerability to dendritic retraction in prefrontal neurones of ageing SAMP10 mouse: a model of cerebral degeneration

Shimada, Atsuyoshi; Tsuzuki, Masako; Keino, Hiromi; Satoh, Mamoru; Chiba, Yoichi; Saitoh, Yuhei; Hosokawa, Masanori

doi:10.1111/j.1365-2990.2006.00632.x

Cited by 61 publications

(48 citation statements)

References 33 publications

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“…[7][8][9][10] Individual neurons in the cerebral cortex of aged SAMP10 mice undergo shrinkage in soma size, dendritic retraction and loss of dendritic spines, resulting in loss of synapses. 11,12 These morphological alterations in cortical neurons are similar to those in the ageing human brain. 1 Age-related progressive neuronal DNA damage has been associated with cerebral degeneration in this model.…”

Section: Introductionmentioning

confidence: 70%

Morphological impairments in microglia precede age-related neuronal degeneration in senescence-accelerated mice

et al. 2011

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The ageing brain is characterized by degenerative changes in both neurons and glia. Although neurons are known to lose dendritic complexity with ageing, age-related changes in the morphology of microglia have not been well documented. We investigated potential age-related changes in microglial morphology using mouse models. Senescence-accelerated mouse prone 10 (SAMP10) in which neuronal degeneration begins to appear around 8 months of age and becomes progressively remarkable with advancing age was used as a model of brain ageing. Senescence-accelerated mouse resistant 1 (SAMR1) in which age-related neuronal changes are inconspicuous was used as usual-ageing controls. Hippocampal sections prepared from 3-, 8- and 14-month-old SAMP10 and 3-, 8-, 14- and 24-month-old SAMR1 mice were stained immunohistochemically with anti-Iba-1 antibody to highlight microglia. Stick figures of individual microglia reflecting the length and complexity of cytoplasmic processes were made by camera lucida drawing. Parameters representing morphological features of microglia were quantified using an image analyzer: area of convex closure, cell body area, number of primary processes, maximal branch order, combined projection length, number of segments and number of tips. Pathological changes of processes such as beading and clusters of fragmented twigs were counted. In microglia of 3- and 8-month-old SAMP10 mice, combined projection length was shorter and numbers of segments and tips were smaller than those in age-matched SAMR1 mice. Similar changes were detected in SAMR1 mice at age 14 months and older. Microglia of SAMP10 mice at all ages were characterized by having frequent pathological changes in processes, which were not remarkable in SAMR1 mice at any age. These morphological abnormalities in microglia of SAMP10 mice preceded the onset of neuronal degeneration and may lead to making brain tissue less protective to neurons. We propose that preceding abnormalities in microglia may contribute to the vulnerability to age-related neuronal degeneration in SAMP10 mice.

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Section: Introductionmentioning

confidence: 70%

Morphological impairments in microglia precede age-related neuronal degeneration in senescence-accelerated mice

et al. 2011

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“…Dendrite retraction and decreased spine density Following previous studies [106,110], which reported that age-related cerebral atrophy in SAMP10 mice was closely associated with loss and perikaryal shrinkage of cortical neurons, they investigated age-related changes in the dendritic arbors and dendritic spines in the medial prefrontal cortex of the SAMP10 mice using a quantitative Golgi method [115]. Dendrites of prefrontal neurons gradually retracted with age towards the soma with the relative preservation of overall complexity, and apical dendrites were much more severely affected than basal dendrites.…”

Section: Neuropathological Studiesmentioning

confidence: 99%

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

Takeda¹

2009

Neurochem Res

217

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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“…The lifespan of the SAMP10 mouse is about a year, and this mouse exhibits encephalatrophy with aging, which is reflected as a learning and memory disorder (Takeda et al 1997). Thus, the SAMP10 mouse is widely used for analysis of mechanisms of aging (Shimada et al 2006;Unno et al 2007;Sasaki et al 2008;Tsuduki et al 2011;Honma et al 2011). In our previous study, we showed that SAMP10 mice fed a standard diet exhibited age-dependent increases of liver hydroxysteroid 11-beta dehydrogenase 1 (Hsd11b1) mRNA level, which promoted insulin secretion and insulin resistance and caused hyperinsulinemia and lipid accumulation in liver and white adipose tissue (Paterson et al 2004;Honma et al 2011).…”

Section: Introductionmentioning

confidence: 98%

High-fat diet intake accelerates aging, increases expression of Hsd11b1, and promotes lipid accumulation in liver of SAMP10 mouse

et al. 2011

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An understanding of the mechanisms of aging is important for prevention of age-related diseases. In this study, we examined age-dependent changes in lipid metabolism in the senescence-accelerated mouse (SAM)P10 fed a high-fat diet to investigate the effects of high-fat intake and aging. Tissue weights and biological parameters in plasma and liver were measured at 6 and 12 months old in SAMP10 mice fed a high-fat diet. These mice showed marked increases in liver triacylglycerol and plasma insulin levels with intake of a high-fat diet intake and aging. Lipid accumulation in hepatocytes and morphological aberrations and hypertrophy in pancreatic islets were also promoted by a high-fat diet and aging. To investigate the underlying mechanisms, the activities and mRNA levels for enzymes associated with lipid metabolism in liver were measured. The results indicated that the lipid metabolic system was activated by a high-fat diet and aging. Liver mRNA level for hydroxysteroid 11-beta dehydrogenase 1 (Hsd11b1), which exhibit age-dependent increases and promote insulin secretion, was also markedly increased. These results suggest that a high-fat diet accelerated aging in the liver of SAMP10 mice by increasing liver mRNA level for Hsd11b1, increasing insulin secretion, and promoting lipid accumulation in the liver.

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Apical vulnerability to dendritic retraction in prefrontal neurones of ageing SAMP10 mouse: a model of cerebral degeneration

Cited by 61 publications

References 33 publications

Morphological impairments in microglia precede age-related neuronal degeneration in senescence-accelerated mice

Morphological impairments in microglia precede age-related neuronal degeneration in senescence-accelerated mice

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

High-fat diet intake accelerates aging, increases expression of Hsd11b1, and promotes lipid accumulation in liver of SAMP10 mouse

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