Calbindin D28k mRNA in hippocampus, superior temporal gyrus and cerebellum: comparison between control and Alzheimer disease subjects

Maguire‐Zeiss, Kathleen A.; Li, Z. W.; Shimoda, Lori M. N.; Hamill, Robert W.

doi:10.1016/0169-328x(95)00035-q

Cited by 26 publications

(15 citation statements)

References 16 publications

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“…Additionally, both probes for calbindin revealed significant decreases (85% and 86%) in hippocampal tissue from AD brains compared with tissue from aged controls brains (data not shown). These findings are in accordance with the idea that calbindin immunoreactivity is reduced in the hippocampus with AD and correlates with pathology, and cognitive impairment (Iritani et al, 2001; Maguire-Zeiss et al, 1995; Palop et al, 2003). On the whole, our results underscore the extent of age-related changes in calcium handling and lend credence to the calcium hypothesis of Alzheimer's disease.…”

Section: Discussionsupporting

confidence: 92%

Age-related downregulation of the CaV3.1 T-type calcium channel as a mediator of amyloid beta production

Rice¹,

Berchtold²,

Cotman³

et al. 2014

Neurobiology of Aging

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Alzheimer's is a crippling neurodegenerative disease that largely affects aged individuals. Decades of research have highlighted age-related changes in calcium homeostasis that occur before and throughout the duration of the disease, and the contributions of such dysregulation to Alzheimer's disease pathogenesis. We report an age-related decrease in expression of the CaV3.1 T-type calcium channel at the level of messenger RNA and protein in both humans and mice that is exacerbated with the presence of Alzheimer's disease. Downregulating T-type calcium channels in N2a cells and the 3xTg-AD mouse model of Alzheimer's disease, by way of pharmacologic inhibition with NNC-55-0396, results in a rapid increase in amyloid beta production via reductions in non-amyloidogenic processing, whereas genetic over-expression of the channel in human embryonic kidney cells expressing amyloid precursor protein produces complementary effects. The age-related decline in CaV3.1 expression may therefore contribute to a pro-amyloidogenic environment in the aging brain and represents a novel opportunity to intervene in the course of Alzheimer's disease pathogenesis.

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Section: Discussionsupporting

confidence: 92%

Age-related downregulation of the CaV3.1 T-type calcium channel as a mediator of amyloid beta production

Rice¹,

Berchtold²,

Cotman³

et al. 2014

Neurobiology of Aging

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show abstract

“…In Alzheimer’s disease, reductions in the number of Calb1-containing neurons were observed in the hippocampal CA2 subfield [18] and various isocortical regions [13] in a layer-specific fashion [11]. In Parkinson’s disease, Calb1-immunoreactive subpopulations of dopaminergic neurons residing in the dorsal substantia nigra pars compacta and ventral tegmental area were relatively spared from degeneration [10, 33].…”

Section: Resultsmentioning

confidence: 99%

Hippocampal calbindin-1 immunoreactivity correlate of recognition memory performance in aged mice

Soontornniyomkij

Risbrough

Young

et al. 2012

Neuroscience Letters

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Aging-related dysregulation of neuronal calcium metabolism, which not only involves the control of calcium fluxes but also the cytosolic calcium buffering system such as calbindin-1 (Calb1), may disturb synaptic plasticity and thereby memory functioning. Calb1 expression has been shown to affect hippocampal long-term potentiation and learning and to play a neuroprotective role in animal models of ischemic brain injury and neurodegenerative disorders. We hypothesize that memory performance in aged mice correlates with neuronal Calb1 protein expression in the hippocampal formation. We studied a set of 18 aged and 22 young male C57BL/6N mice, in which the aged group performed poorer than the young in single-trial novel object recognition testing (two-tailed p=0.005, U test). Apparent decreases in the Calb1 immunoreactivity (measured by quantitative immunohistochemistry) in aged mice compared to that in young mice were not statistically significant either in the hippocampal CA1 subfield or dentate gyrus. In the aged mouse group, levels of Calb1 immunoreactivity both in the CA1 subfield and dentate gyrus correlated directly with the measure of recognition memory performance (Spearman rank correlation rs=0.47 and 0.48, two-tailed p=0.047 and 0.044, respectively). Our results suggest that hippocampal Calb1 expression affects memory performance in aged mice probably via its role in maintaining neuronal calcium homeostasis. Alternatively, our finding of lower Calb1 immunoreactivity with poorer memory performance in aged mice might be attributed to saturation of Calb1 protein by higher levels of intracellular calcium, due to aging-related dysregulation of neuronal calcium fluxes.

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“…(67) In some neurons, analogous to the antiapoptotic effect of calbindin-D 28k in lymphocytes, (68) the induction of calbindins by 1,25(OH) 2 D 3 may protect against cell death in the face of repetitive calcium transients, (69) and in fact the expression of calbindin-D 28k mRNA is decreased in the hippocampus of Alzheimer's patients as assessed by in situ hybridization. (70,71) Taken together, these observations not only imply a modulatory role for VDR in neural cell growth and differentiation but also intimate a possible role for 1,25(OH) 2 57) suppression of ␥-interferon (202) and IL-1 through IL-6 (53,159,203) Central nervous system dorsal root ganglia, (204) glial cells, and hippocampus (70,107) production of NGF, (65,66,205) neurotrophin-3, (64) and leukemia inhibitory factor (63) Epithelium epidermal skin/keratinocyte (206) differentiation (17,211) hair follicle (207) differentiation (16,17,212) female reproductive tract (208) uterine development (16) mammary (108) 2 cell growth (213) prostate (209) 2 cell growth (173) colon (210) 2 cell growth (170,214) lung (108) surfactant (215) Endocrine system thyrotrope (216) TRH receptor (218) thyroid (108) 2...…”

Section: Neoclassical 125(oh) 2 D 3 /Vdr Actionsmentioning

confidence: 99%

The Nuclear Vitamin D Receptor: Biological and Molecular Regulatory Properties Revealed

Haussler

Whitfield

Haussler

et al. 1998

Journal of Bone and Mineral Research

1,267

890

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Calbindin D28k mRNA in hippocampus, superior temporal gyrus and cerebellum: comparison between control and Alzheimer disease subjects

Cited by 26 publications

References 16 publications

Age-related downregulation of the CaV3.1 T-type calcium channel as a mediator of amyloid beta production

Age-related downregulation of the CaV3.1 T-type calcium channel as a mediator of amyloid beta production

Hippocampal calbindin-1 immunoreactivity correlate of recognition memory performance in aged mice

The Nuclear Vitamin D Receptor: Biological and Molecular Regulatory Properties Revealed

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