Reduction of calbindin-28k mRNA levels in Alzheimer as compared to Huntington hippocampus

Sutherland, May Kung; Wong, Lee Jun; Somerville, Martin J.; Yoong, Larry K.K.; Bergeron, Catherine; Parmentier, Marc; McLachlan, Donald R.

doi:10.1016/0169-328x(93)90171-k

Cited by 46 publications

(22 citation statements)

References 47 publications

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“…Cal is a neuronal calcium binding protein, which may act as a buffer for neuronal calcium. Cal-positive pyramidal cells do not accumulate NFT in AD, which suggests that loss of Cal expression in specific hippocampal neuronal populations may be associated with reduced resistance to injury and loss [116]. Previous work in our laboratory demonstrated an age-related and significant loss of Cal immune-reactive neurons in the hippocampal CA1 region in Ts65Dn mice (Fig.…”

Section: Neuronal Cell Lossmentioning

confidence: 82%

Cognitive Impairment, Neuroimaging, and Alzheimer Neuropathology in Mouse Models of Down Syndrome

Hamlett¹,

Boger²,

Ledreux³

et al. 2015

CAR

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Down syndrome (DS) is the most common non-lethal genetic condition that affects approximately 1 in 700 births in the United States of America. DS is characterized by complete or segmental chromosome 21 trisomy, which leads to variable intellectual disabilities, progressive memory loss, and accelerated neurodegeneration with age. During the last three decades, people with DS have experienced a doubling of life expectancy due to progress in treatment of medical comorbidities, which has allowed this population to reach the age when they develop early onset Alzheimer’s disease (AD). Individuals with DS develop cognitive and pathological hallmarks of AD in their fourth or fifth decade, and are currently lacking successful prevention or treatment options for dementia. The profound memory deficits associated with DS-related AD (DS-AD) have been associated with degeneration of several neuronal populations, but mechanisms of neurodegeneration are largely unexplored. The most successful animal model for DS is the Ts65Dn mouse, but several new models have also been developed. In the current review, we discuss recent findings and potential treatment options for the management of memory loss and AD neuropathology in DS mouse models. We also review age-related neuropathology, and recent findings from neuroimaging studies. The validation of appropriate DS mouse models that mimic neurodegeneration and memory loss in humans with DS can be valuable in the study of novel preventative and treatment interventions, and may be helpful in pinpointing gene-gene interactions as well as specific gene segments involved in neurodegeneration.

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Section: Neuronal Cell Lossmentioning

confidence: 82%

Cognitive Impairment, Neuroimaging, and Alzheimer Neuropathology in Mouse Models of Down Syndrome

Hamlett¹,

Boger²,

Ledreux³

et al. 2015

CAR

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“…One important function of calbindin is its role as an intraneuronal calcium buffering system, which helps prevent toxic accumulation of cytosolic-free calcium (26)(27)(28)(29). Alterations in calcium binding proteins are evident following acute central nervous system insult as well as chronic neurodegenerative disorders, such as Alzheimer disease (27)(28)(29). Recent studies have proposed calcium influx as an important mediator in the pathogenesis of HIV-associated neurological damage (30).…”

Section: Discussionmentioning

confidence: 99%

Progressive decline in avoidance learning paralleled by inflammatory neurodegeneration in transgenic mice expressing interleukin 6 in the brain

Heyser

Masliah

Samimi

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

346

206

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Inf lammation with expression of interleukin 6 (IL-6) in the brain occurs in many neurodegenerative disorders. To better understand the role of IL-6 in such disorders, we examined performance in a learning task in conjunction with molecular and cellular neuropathology in transgenic mice that express IL-6 chronically from astrocytes in the brain. Transgenic mice exhibited dose-and age-related deficits in avoidance learning that closely corresponded with specific progressive neuropathological changes. These results establish a link between the central nervous system expression of IL-6, inf lammatory neurodegeneration, and a learning impairment in transgenic mice. They suggest a critical role for a proinf lammatory cytokine in the cognitive deficits and associated neuroinf lammatory changes that have been documented in neurodegenerative diseases such as Alzheimer disease and AIDS.

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“…Among the behavioral difficulties patients experience are issues involving executive function, emotionality, reasoning, and motor skills, all of which are mediated by the FC and/or CB functions [64,65]. A reduction in Calb1 gene and/or protein expression has been detected in brains of patients who suffered from an assortment of neurodegenerative diseases [66,67,68], and several neurobehavioral disorders are correlated with decreased size and/or numbers of Purkinje cells [69,70]. Sex differences in these brain regions in normal animals, such as those reported here, could provide clues underlying the etiologies of these diseases.…”

Section: Discussionmentioning

confidence: 99%

Sex Differences in the Cerebellum and Frontal Cortex: Roles of Estrogen Receptor Alpha and Sex Chromosome Genes

Abel¹,

Witt²,

Rissman³

2011

Neuroendocrinology

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Most neurobehavioral diseases are sexually dimorphic in their incidence, and sex differences in the brain may be key for understanding and treating these diseases. Calbindin (Calb) D28K is used as a biomarker for the well-studied sexually dimorphic nucleus, a hypothalamic structure that is larger in males than in females. In the current study weanling C56BL/6J mice were used to examine sex differences in the Calb protein and message focusing on regions outside of the hypothalamus. A robust sex difference was found in Calb in the frontal cortex (FC) and cerebellum (CB; specifically in Purkinje cells); mRNA and protein were higher in females than in males. Using 2 mouse lines, i.e. one with a complete deletion of estrogen receptor alpha (ERα) and the other with uncoupled gonads and sex chromosomes, we probed the mechanisms that underlie sexual dimorphisms. In the FC, deletion of ERα reduced Calb1 mRNA in females compared to males. In addition, females with XY sex chromosomes had levels of Calb1 equal to those of males. Thus, both ERα and the sex chromosome complement regulate Calb1 in the FC. In the CB, ERα knockout mice of both sexes had reduced Calb1 mRNA, yet sex differences were retained. However, the sex chromosome complement, regardless of gonadal sex, dictated Calb1 mRNA levels. Mice with XX chromosomes had significantly greater Calb1 than did XY mice. This is the first study demonstrating that sex chromosome genes are a driving force producing sex differences in the CB and FC, which are neuoranatomical regions involved in many normal functions and in neurobehavioral diseases.

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Reduction of calbindin-28k mRNA levels in Alzheimer as compared to Huntington hippocampus

Cited by 46 publications

References 47 publications

Cognitive Impairment, Neuroimaging, and Alzheimer Neuropathology in Mouse Models of Down Syndrome

Cognitive Impairment, Neuroimaging, and Alzheimer Neuropathology in Mouse Models of Down Syndrome

Progressive decline in avoidance learning paralleled by inflammatory neurodegeneration in transgenic mice expressing interleukin 6 in the brain

Sex Differences in the Cerebellum and Frontal Cortex: Roles of Estrogen Receptor Alpha and Sex Chromosome Genes

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