Magnetic Resonance Imaging as a Tool for the Study of Mouse Models of Autism

Ellegood, Jacob; Henkelman, R. Mark; Lerch, Jason P.

doi:10.4172/2165-7890.s1-008

Cited by 2 publications

(3 citation statements)

References 70 publications

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“…Some models such as a Rett syndrome mouse model have shown quite comparable neuroanatomical alterations as are observed in human patients (Ellegood, 2012). Phelan-McDermid syndrome, which oftentimes goes along with a syndromal variant of ASD, is a SHANK3 deficiency disorder and patients frequently have low zinc levels, which can be a modifying factor of their phenotype (Pfaender et al, 2017).…”

Section: Discussionmentioning

confidence: 91%

“…Genetic alterations account for approximately two thirds of all cases (Huguet et al, 2016), and studies on identical twins show high concordance rates with strong penetrance of mutations. We know some of the genetic factors, however, the number of possible mutations is daunting with hundreds of genes potentially contributing to the phenotype (Ellegood, 2012). Nevertheless, there is a large cluster of genes coding for synaptic proteins.…”

Section: Introductionmentioning

confidence: 99%

“…The detailed volumetric deviation of specific parts of the brain is highly heterogeneous, which is attributable to age, intelligence quotient, but predominantly to the underlying genetic alterations. To reduce this factor, it has been reasoned to analyze neuroanatomy of syndromal ASD in humans and to model the different disease entities in mouse models, which allow for a specific genotype-phenotype correlation (Ellegood, 2012).…”

Section: Introductionmentioning

confidence: 99%

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Shank3 Transgenic and Prenatal Zinc-Deficient Autism Mouse Models Show Convergent and Individual Alterations of Brain Structures in MRI

Schoen

Asoglu

Bauer

et al. 2019

Front. Neural Circuits

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Research efforts over the past decades have unraveled both genetic and environmental factors, which contribute to the development of autism spectrum disorders (ASD). It is, to date, largely unknown how different underlying causes result in a common phenotype. However, the individual course of development and the different comorbidities might reflect the heterogeneous genetic and non-genetic contributions. Therefore, it is reasonable to identify commonalities and differences in models of these disorders at the different hierarchical levels of brain function, including genetics/environment, cellular/synaptic functions, brain regions, connectivity, and behavior. To that end, we investigated Shank3 transgenic mouse lines and compared them with a prenatal zinc-deficient (PZD) mouse model of ASD at the level of brain structural alterations in an 11,7 T small animal magnetic resonance imaging (MRI). Animals were measured at 4 and 9 weeks of age. We identified a decreased total brain volume (TBV) and hippocampal size of Shank3 −/− mice but a convergent increase of basal ganglia (striatum and globus pallidus) in most mouse lines. Moreover, Shank3 transgenic mice had smaller thalami, whereas PZD mice had this region enlarged. Intriguingly, Shank3 heterozygous knockout mice mostly showed minor abnormalities to full knockouts, which might reflect the importance of proper Shank3 dosage in neuronal cells. Most reported volume changes seemed to be more pronounced at younger age. Our results indicate both convergent and divergent brain region abnormalities in genetic and non-genetic models of ASD. These alterations of brain structures might be mirrored in the reported behavior of both models, which have not been assessed in this study.

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Section: Discussionmentioning

confidence: 91%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Shank3 Transgenic and Prenatal Zinc-Deficient Autism Mouse Models Show Convergent and Individual Alterations of Brain Structures in MRI

Schoen

Asoglu

Bauer

et al. 2019

Front. Neural Circuits

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Delayed parenthood and its influence on offspring health: what have we learned from the mouse model

Zacchini¹,

Sampino²,

Zietek³

et al. 2021

Biology of Reproduction

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Delayed parenthood is constantly increasing worldwide due to various socio-economic factors. In the last decade, a growing number of epidemiological studies have suggested a link between advanced parental age and an increased risk of diseases in the offspring. Also, poor reproductive outcome has been described in pregnancies conceived by aged parents. Similarly, animal studies showed that aging negatively affects gametes, early embryonic development, pregnancy progression and the postnatal phenotype of resulting offspring. However, how and to what extent parental age is a risk factor for the health of future generations is still subject to debate. Notwithstanding the limitation of an animal model, the mouse model represents a useful tool to understand not only the influence of parental age on offspring phenotype but also the biological mechanisms underlying the poor reproductive outcome and the occurrence of diseases in the descendants. The present review aims at i) providing an overview of the current knowledge from mouse model about the risks associated with conception at advanced age (e.g. neurodevelopmental and metabolic disorders), ii) highlighting the candidate biological mechanisms underlying this phenomenon, and iii) discussing on how murine-derived data can be relevant to humans.

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Magnetic Resonance Imaging as a Tool for the Study of Mouse Models of Autism

Cited by 2 publications

References 70 publications

Shank3 Transgenic and Prenatal Zinc-Deficient Autism Mouse Models Show Convergent and Individual Alterations of Brain Structures in MRI

Shank3 Transgenic and Prenatal Zinc-Deficient Autism Mouse Models Show Convergent and Individual Alterations of Brain Structures in MRI

Delayed parenthood and its influence on offspring health: what have we learned from the mouse model

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