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1. Estropause, sex hormones and metal homeostasis in the mouse brain

Author

Liu, Tianbing, Bowen, Richard L., Wilson, Andrea C., Atwood, Craig S., Liu, Tianbing, Bowen, Richard L., Wilson, Andrea C., and Atwood, Craig S.

Abstract

Alterations in brain metal ion homeostasis have been reported with aging and are implicated in the pathogenesis of neurodegenerative diseases. To assess whether age-related changes in hypothalamic-pituitary-gonadal (HPG) hormones might be involved in modulating brain metal ion homeostasis, we treated 7.5-month intact, sham-ovariecomized and ovariectomized C57B6SJL mice with vehicle or leuprolide acetate (for 9-months) to differentiate between whether sex steroids or gonadotropins might modulate brain metal ion concentrations. Unlike other aging mammals, there was no increase in plasma luteinizing hormone (LH) and follicle-stimulating hormone (FSH) concentrations following estropause in mice, suggesting there was sufficient residual production by the follicle depleted ovary, of sex steroids like estrogens and protein hormones like the inhibins, in order to suppress pituitary LH/FSH production. Castration on the other hand induced significant increases in circulating LH and FSH. Modulation of plasma sex steroid and gonadotropin levels did not significantly alter the concentrations of brain metals tested (Fe, Zn, Cu, Mn, Co, Ni, Al, Li), although there was a tendency for a decrease in all brain metals following ovariectomy (low estrogens and progesterone, high gonadotropins), a response that was reversed with leuprolide acetate treatment (low sex steroids, low gonadotropins). Brain Cu concentration was the only metal correlated with plasma LH (−0.37, n = 30, p < 0.05) and FSH (−0.42, n = 29, p < 0.01). This study demonstrates that sex hormones do not markedly alter brain metal ion homeostasis, unlike previously reported studies of circulating metal ion homeostasis. The role of gonadotropins in regulating metal ion homeostasis does however warrant further study.

Published
2022

7. Activin Receptor Signaling Regulates Prostatic Epithelial Cell Adhesion and Viability1

Author

Simon, Derek P, Vadakkadath Meethal, Sivan, Wilson, Andrea C, Gallego, Miguel J, Weinecke, Stephanie L, Bruce, Erin, Lyons, Patrick F, Haasl, Ryan J, Bowen, Richard L, and Atwood, Craig S

Subjects
Male, Cell Survival, Activin Receptors, Type II, Immunoblotting, Membrane Proteins, Prostatic Neoplasms, Epithelial Cells, Activins, ADAM Proteins, Neuroblastoma, Cell Line, Tumor, Cell Adhesion, Humans, Research Article, Signal Transduction
Abstract

Mutational changes coupled with endocrine, paracrine, and/or autocrine signals regulate cell division during carcinogenesis. The hormone signals remain undefined, although the absolute requirement in vitro for fetal serum indicates the necessity for a fetal serum factor(s) in cell proliferation. Using prostatic cancer cell (PCC) lines as a model of cancer cell proliferation, we have identified the fetal serum component activin A and its signaling through the activin receptor type II (ActRII), as necessary, although not sufficient, for PCC proliferation. Activin A induced Smad2 phosphorylation and PCC proliferation, but only in the presence of fetal bovine serum (FBS). Conversely, activin A antibodies and inhibin A suppressed FBS-induced PCC proliferation confirming activin A as one of multiple serum components required for PCC proliferation. Basic fibroblast growth factor was subsequently shown to synergize activin A-induced PCC proliferation. Inhibition of ActRII signaling using a blocking antibody or antisense-P decreased mature ActRII expression, Smad2 phosphorylation, and the apparent viability of PCCs and neuroblastoma cells grown in FBS. Suppression of ActRII signaling in PCC and neuroblastoma cells did not induce apoptosis as indicated by the ratio of active/inactive caspase 3 but did correlate with increased cell detachment and ADAM-15 expression, a disintegrin whose expression is strongly correlated with prostatic metastasis. These findings indicate that ActRII signaling is required for PCC and neuroblastoma cell viability, with ActRII mediating cell fate via the regulation of cell adhesion. That ActRII signaling governs both cell viability and cell adhesion has important implications for developing therapeutic strategies to regulate cancer growth and metastasis.

Published
2009

8. The acceleration of aging and Alzheimer’s disease through the biological mechanisms behind obesity and type II diabetes

Author

Martins, Ian J, Lim, Wei Ling F, Wilson, Andrea C, Laws, Simon M, Martins, Ralph, Martins, Ian J, Lim, Wei Ling F, Wilson, Andrea C, Laws, Simon M, and Martins, Ralph

Abstract

The incidence of diabetes is predicted to increase to 21% by 2050. Currently, one third of US adults are obese and over 11% of these individuals have diabetes. Due to the growing need for therapeutic intervention to control and/or stabilize this increase in the incidence of diabetes in Western communities, gaining a comprehensive understanding of the association between obesity and Type 2 diabetes has become increasingly important to diabetes research. The increased cell senescence associated with diabetes has been associated with the limited ability of cells to divide, with indication of telomere shortening and genomic instability of the cells. Obese individuals have shorter telomeres suggesting an inverse relationship between adiposity and telomere length. The implication that Type 2 diabetes has on biological aging is of particular interest since telomere shortening in obesity and diabetes has been associated with an early risk for dementia and even progression to Alzheimer’s disease (AD). Lifestyle, nutrition and longevity are closely related and cellular senescence has been associated with telomere shortening and connected to longevity. Diet, cholesterol lowering drugs and exercise that control food intake and glucose tolerance in aging and diabetic individuals, via connections between liver circadian clocks and the suprachiasmatic nucleus in the brain, also have been shown to alter telomere lengths. Lifestyle interventions, such as diets low in fat and exercise, target the rise in obesity and associated telomere shortening by delaying or preventing the onset of Type 2 diabetes. The implementation of these anti-aging therapies early in life may prevent calorie overload and activation of calorie sensitive genes such as Sirtuin 1 (Sirt1). This may maintain telomere length and the control of obesity, which is linked to cardiovascular disease, diabetes and accelerates aging and AD.

Published
2013

9. Follow-up plasma apolipoprotein E levels in the Australian Imaging, Biomarkers and Lifestyle Flagship Study of Ageing (AIBL) cohort.

Author

Gupta, Veer B., Wilson, Andrea C., Burnham, Samantha, Hone, Eugene, Pedrini, Steve, Laws, Simon M., Wei Ling Florence Lim, Rembach, Alan, Rainey-Smith, Stephanie, Ames, David, Cobiac, Lynne, Macaulay, S. Lance, Masters, Colin L., Rowe, Christopher C., Bush, Ashley I., and Martins, Ralph N.

Subjects
*ALZHEIMER'S disease prevention, *FOLLOW-up studies (Medicine), *APOLIPOPROTEIN E, *BIOMARKERS, *SOCIOECONOMICS, *ETIOLOGY of diseases
Abstract

Introduction: Alzheimer's disease (AD) is a growing socioeconomic problem worldwide. Early diagnosis and prevention of this devastating disease have become a research priority. Consequently, the identification of clinically significant and sensitive blood biomarkers for its early detection is very important. Apolipoprotein E (APOE) is a well-known and established genetic risk factor for late-onset AD; however, the impact of the protein level on AD risk is unclear. We assessed the utility of plasma ApoE protein as a potential biomarker of AD in the large, well-characterised Australian Imaging, Biomarkers and Lifestyle Study of Ageing (AIBL) cohort. Methods: Total plasma ApoE levels were measured at 18-month follow-up using a commercial bead-based enzyme-linked immunosorbent assay: the Luminex xMAP human apolipoprotein kit. ApoE levels were then analysed between clinical classifications (healthy controls, mild cognitive impairment (MCI) and AD) and correlated with the data available from the AIBL cohort, including but not limited to APOE genotype and cerebral amyloid burden. Results: A significant decrease in ApoE levels was found in the AD group compared with the healthy controls. These results validate previously published ApoE protein levels at baseline obtained using different methodology. ApoE protein levels were also significantly affected, depending on APOE genotypes, with e2/e2 having the highest protein levels and e4/e4 having the lowest. Plasma ApoE levels were significantly negatively correlated with cerebral amyloid burden as measured by neuroimaging. Conclusions: ApoE is decreased in individuals with AD compared with healthy controls at 18-month follow-up, and this trend is consistent with our results published at baseline. The influence of APOE genotype and sex on the protein levels are also explored. It is clear that ApoE is a strong player in the aetiology of this disease at both the protein and genetic levels. [ABSTRACT FROM AUTHOR]

Published
2015
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10. Interactions between Apo E and amyloid beta and their relationship to nutriproteomics and neurodegeneration

Author

Martins, Ian J, Gupta, Veer, Wilson, Andrea C, Fuller, Stephanie J, Martins, Ralph N, Martins, Ian J, Gupta, Veer, Wilson, Andrea C, Fuller, Stephanie J, and Martins, Ralph N

Abstract

Martins I.J., Gupta V., Wilson A.C., Fuller S.J., Martins R.N. (2014). Interactions between Apo E and amyloid beta and their relationship to nutriproteomics and neurodegeneration. Current Proteomics, 11(3), 171-183. Available here

11. Follow-up Plasma Apolipoprotein e Levels In The Australian Imaging, Biomarkers And Lifestyle Flagship Study of Ageing (AIBL) Cohort

Author

Gupta, V.B, Veer B., Wilson, Andrea C., Burnham, Samantha, Hone, Eugene, Pedrini, Steve, Laws, Simon M, Lim, Wei L.F., Rembach, Alan, Rainey-Smith, Stephanie, Ames, David, Cobiac, Lynne, MacAulay, S L., Masters, Colin L., Rowe, Christopher C., Bush, Ashley I, Martins, Ralph, AIBL Research Group, Gupta, V.B, Veer B., Wilson, Andrea C., Burnham, Samantha, Hone, Eugene, Pedrini, Steve, Laws, Simon M, Lim, Wei L.F., Rembach, Alan, Rainey-Smith, Stephanie, Ames, David, Cobiac, Lynne, MacAulay, S L., Masters, Colin L., Rowe, Christopher C., Bush, Ashley I, Martins, Ralph, and AIBL Research Group

Abstract

Gupta, V. B., Wilson, A. C., Burnham, S., Hone, E., Pedrini, S., Laws, S. M., ... & Martins, R. N. (2015). Follow-up plasma apolipoprotein E levels in the Australian Imaging, Biomarkers and Lifestyle Flagship Study of Ageing (AIBL) cohort. Alzheimer's research & therapy, 7(1), 16. Available http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made Available in this article, unless otherwise stated.

12. TDP-43 in aging and Alzheimer's disease - a review.

Author

Wilson AC, Dugger BN, Dickson DW, and Wang DS

Subjects
Aged, Aged, 80 and over, Aging genetics, Alzheimer Disease genetics, Alzheimer Disease pathology, DNA-Binding Proteins genetics, Humans, Motor Neurons pathology, TDP-43 Proteinopathies genetics, TDP-43 Proteinopathies pathology, Aging metabolism, Alzheimer Disease metabolism, DNA-Binding Proteins metabolism, Motor Neurons metabolism, TDP-43 Proteinopathies metabolism
Abstract

Transactive response DNA-binding protein of 43 kDa (TDP-43), an RNA and DNA binding protein involved in transcriptional repression, RNA splicing and RNA metabolism during the stress response, is the major component of neuronal inclusions in amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration with ubiquitin inclusions, now referred to as FTLD-TDP. While initially thought to be relatively specific to ALS and FTLD-TDP, TDP-43 pathology has now been detected in a number of other neurodegenerative diseases, many associated with tau pathology, including Guam Parkinson dementia complex and Alzheimer's disease (AD). TDP-43 pathology is detected in 25% to 50% of AD cases, especially those with more severe clinical phenotype and greater Alzheimer type pathology, as well as AD cases with hippocampal sclerosis (HS). HS is characterized by selective neuronal loss affecting CA1 sector of the hippocampus, and most cases of HS, with or without AD, have TDP-43 pathology. Whether TDP-43 pathology is merely an incidental finding in AD or actually contributing to the more severe clinical phenotype remains unresolved. Presence of TDP-43 in normal elderly, who are at increased risk for AD, would strengthen the argument that it is not merely a secondary or incidental finding in end stage AD. Limited studies suggest that TDP-43 pathology is infrequent in neurologically normal elderly (3% or less). We provide an overview of what is known about TDP-43 in AD, normal aging and in other disorders and suggest that TDP-43 proteinopathies be considered in two classes - primary and secondary.

Published
2011

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