Serum calcium levels and neuropsychological performance in depression and matched healthy controls: Reversal of correlation a marker of the aging cognitive clock?

Grützner, Thea Marianne; Listunova, Lena; Fabian, Gregor Amadeus; Kramer, Benedikt Alexander; Flach, Daniel; Weisbrod, Matthias; Roesch-Ely, Daniela; Sharma, Anuradha

doi:10.1016/j.psyneuen.2018.03.012

Cited by 19 publications

(11 citation statements)

References 39 publications

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“…by SKAT analysis do not provide directionality, but the risks of embolism/ thrombosis and diastolic heart failure have been shown to be influenced by serum Ca concentrations; 32,33 likewise, neuropsychiatric disorders have been associated with serum Ca concentrations in small case-control studies. 34,35 CaSR is widely expressed in the cardiovascular 36,37 and nervous 38 systems, and it remains to be determined whether these disease associations result from elevated serum Ca concentrations, reduced CaSR function, or both.…”

Section: Discussionmentioning

confidence: 99%

Familial Hypocalciuric Hypercalcemia Type 1 and Autosomal-Dominant Hypocalcemia Type 1: Prevalence in a Large Healthcare Population

Dershem

Gorvin

Metpally

et al. 2020

The American Journal of Human Genetics

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The calcium-sensing receptor (CaSR) regulates serum calcium concentrations. CASR loss-or gain-of-function mutations cause familial hypocalciuric hypercalcemia type 1 (FHH1) or autosomal-dominant hypocalcemia type 1 (ADH1), respectively, but the population prevalence of FHH1 or ADH1 is unknown. Rare CASR variants were identified in whole-exome sequences from 51,289 de-identified individuals in the DiscovEHR cohort derived from a single US healthcare system. We integrated bioinformatics pathogenicity triage, mean serum Ca concentrations, and mode of inheritance to identify potential FHH1 or ADH1 variants, and we used a Sequence Kernel Association Test (SKAT) to identify rare variant-associated diseases. We identified predicted heterozygous loss-of-function CASR variants (6 different nonsense/frameshift variants and 12 different missense variants) in 38 unrelated individuals, 21 of whom were hypercalcemic. Missense CASR variants were identified in two unrelated hypocalcemic individuals. Functional studies showed that all hypercalcemiaassociated missense variants impaired heterologous expression, plasma membrane targeting, and/or signaling, whereas hypocalcemiaassociated missense variants increased expression, plasma membrane targeting, and/or signaling. Thus, 38 individuals with a genetic diagnosis of FHH1 and two individuals with a genetic diagnosis of ADH1 were identified in the 51,289 cohort, giving a prevalence in this population of 74.1 per 100,000 for FHH1 and 3.9 per 100,000 for ADH1. SKAT combining all nonsense, frameshift, and missense loss-of-function variants revealed associations with cardiovascular, neurological, and other diseases. In conclusion, FHH1 is a common cause of hypercalcemia, with prevalence similar to that of primary hyperparathyroidism, and is associated with altered disease risks, whereas ADH1 is a major cause of non-surgical hypoparathyroidism.

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Section: Discussionmentioning

confidence: 99%

Familial Hypocalciuric Hypercalcemia Type 1 and Autosomal-Dominant Hypocalcemia Type 1: Prevalence in a Large Healthcare Population

Dershem

Gorvin

Metpally

et al. 2020

The American Journal of Human Genetics

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“…The serum calcium homeostasis is controlled by hormones such as parathyroid hormone (PTH) and calcitonin [23]. Serum calcium concentration has been reported to be associated with depression and schizophrenia and is a reported biomarker of psychiatric disorders [15, 32, 42]. Payne et al [32] reported that serum calcium concentrations within the physiological standard range are correlated with neuropsychological performance.…”

Section: Discussionmentioning

confidence: 99%

Effects of housing conditions on behaviors and biochemical parameters in juvenile cynomolgus monkeys (<i>Macaca fascicularis</i>)

et al. 2019

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To investigate the effects of environmental enrichment on laboratory monkeys, we studied behavioral and physiological differences following changes in housing conditions. Ten male and female juvenile cynomolgus monkeys were first housed in pairs for 8 weeks after quarantine/acclimatization (singly housed) and subsequently housed alone for the next 8 weeks. Monkeys were subjected to evaluations of body weight gain, stereotypic or affiliative behaviors, cortisol, 4-ethylphenyl sulfate (4EPS) and catecholamine concentrations in biological samples, and blood chemistry tests under both housing conditions. Under paired housing, the stereotypic behavioral score decreased in both sexes, and the affiliative behavioral score increased in males and showed an increasing trend in females. Under single housing, the stereotypic score increased in both sexes, and the affiliative score decreased in males. Paired housing decreased serum calcium and urine cortisol concentrations in both sexes and decreased plasma cortisol in males and plasma 4EPS concentrations in females. The stereotypic score was positively correlated with serum calcium, plasma and urine cortisol, and plasma 4EPS concentration and negatively correlated with the affiliative score. The feces painting score, affiliative score, and plasma cortisol and serum calcium concentrations showed sex differences, suggesting differences in responsiveness to environmental changes between males and females. In conclusion, paired housing improved behavioral abnormalities in juvenile cynomolgus monkeys, suggesting that it may be an effective environmental enrichment paradigm. Calcium, cortisol, and 4EPS concentrations in biological samples may be useful indices for evaluating the effects of environmental enrichment.

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“…Tight regulation of calcium signaling is critical for many important functions of the brain, and subtle impairment in calcium signaling or disturbed calcium homeostasis can result in deleterious consequences including neuronal death [32] and age-related cognitive decline [33][34][35]. DM increases the risk of developing renal failure and contributes to impediment to phosphorus excretion from kidney, and thus leads to hyperphosphatemia.…”

Section: Diabetes Enhanced Ca 2+ Dysregulation Is a Vital Pathogenic mentioning

confidence: 99%

Potential Biochemical Mechanisms of Brain Injury in Diabetes Mellitus

Xing¹,

Tang²,

Lei³

et al. 2020

Aging and disease

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The goal of this review was to summarize current biochemical mechanisms of and risk factors for diabetic brain injury. We mainly summarized mechanisms published in the past three years and focused on diabetes induced cognitive impairment, diabetes-linked Alzheimer's disease, and diabetic stroke. We think there is a need to conduct further studies with increased sample sizes and prolonged period of follow-ups to clarify the effect of DM on brain dysfunction. Additionally, we also think that enhancing experimental reproducibility using animal models in conjunction with application of advanced devices should be considered when new experiments are designed. It is expected that further investigation of the underlying mechanisms of diabetic cognitive impairment will provide novel insights into therapeutic approaches for ameliorating diabetes-associated injury in the brain.

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Serum calcium levels and neuropsychological performance in depression and matched healthy controls: Reversal of correlation a marker of the aging cognitive clock?

Cited by 19 publications

References 39 publications

Familial Hypocalciuric Hypercalcemia Type 1 and Autosomal-Dominant Hypocalcemia Type 1: Prevalence in a Large Healthcare Population

Familial Hypocalciuric Hypercalcemia Type 1 and Autosomal-Dominant Hypocalcemia Type 1: Prevalence in a Large Healthcare Population

Effects of housing conditions on behaviors and biochemical parameters in juvenile cynomolgus monkeys (<i>Macaca fascicularis</i>)

Potential Biochemical Mechanisms of Brain Injury in Diabetes Mellitus

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