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Martins I.J.,Edith Cowan University | Martins I.J.,The University ofWestern Australia | Martins I.J.,McCusker Alzheimers Research Foundation
International Journal of Molecular Sciences | Year: 2015

Chronic neurodegenerative diseases are now associated with obesity and diabetes and linked to the developing and developed world. Interests in healthy diets have escalated that may prevent neurodegenerative diseases such as Parkinson’s and Alzheimer’s disease. The global metabolic syndrome involves lipoprotein abnormalities and insulin resistance and is the major disorder for induction of neurological disease. The effects of bacterial lipopolysaccharides (LPS) on dyslipidemia and NAFLD indicate that the clearance and metabolism of fungal mycotoxins are linked to hypercholesterolemia and amyloid beta oligomers. LPS and mycotoxins are associated with membrane lipid disturbances with effects on cholesterol interacting proteins, lipoprotein metabolism, and membrane apo E/amyloid beta interactions relevant to hypercholesterolemia with close connections to neurological diseases. The influence of diet on mycotoxin metabolism has accelerated with the close association between mycotoxin contamination from agricultural products such as apple juice, grains, alcohol, and coffee. Cholesterol efflux in lipoproteins and membrane cholesterol are determined by LPS with involvement of mycotoxin on amyloid beta metabolism. Nutritional interventions such as diets low in fat/carbohydrate/cholesterol have become of interest with relevance to low absorption of lipophilic LPS and mycotoxin into lipoproteins with rapid metabolism of mycotoxin to the liver with the prevention of neurodegeneration. © 2015 by the authors; licensee MDPI, Basel, Switzerland.

Brown B.M.,University of Western Australia | Brown B.M.,Edith Cowan University | Brown B.M.,McCusker Alzheimers Research Foundation | Peiffer J.J.,Murdoch University | And 3 more authors.
Molecular Psychiatry | Year: 2013

Western countries are experiencing aging populations and increased longevity; thus, the incidence of dementia and Alzheimer's disease (AD) in these countries is projected to soar. In the absence of a therapeutic drug, non-pharmacological preventative approaches are being investigated. One of these approaches is regular participation in physical activity or exercise. This paper reviews studies that have explored the relationship between physical activity and cognitive function, cognitive decline, AD/dementia risk and AD-associated biomarkers and processes. There is now strong evidence that links regular physical activity or exercise to higher cognitive function, decreased cognitive decline and reduced risk of AD or dementia. Nevertheless, these associations require further investigation, more specifically with interventional studies that include long follow-up periods. In particular, relatively little is known about the underlying mechanism(s) of the associations between physical activity and AD neuropathology; clearly this is an area in need of further research, particularly in human populations. Although benefits of physical activity or exercise are clearly recognised, there is a need to clarify how much physical activity provides the greatest benefit and also whether people of different genotypes require tailored exercise regimes. © 2013 Macmillan Publishers Limited.

Hare D.J.,University of Technology, Sydney | Hare D.J.,University of Melbourne | Faux N.G.,University of Melbourne | Faux N.G.,IBM | And 8 more authors.
Metallomics | Year: 2016

We examined serum and erythrocyte lead and manganese levels in the Australian Imaging, Biomarkers and Lifestyle Flagship Study of Ageing (AIBL), which contains over 1000 registrants including over 200 cases of Alzheimer's disease (AD) and 100 mildly cognitively impaired (MCI) individuals. After correcting for confounding effects of age, collection site and sex, we found a significant decrease in serum manganese levels in AD subjects compared to healthy controls. Analysis of smaller subset of erythrocytes revealed no difference in either lead or manganese levels in AD. Although lead and manganese have neurotoxic effects and may be involved in AD pathology, our results showed that neither metal in serum nor erythrocytes are suitable biomarkers in our cohort. However, prospective studies might reveal whether the burden of either metal modifies disease outcomes. © 2016 The Royal Society of Chemistry.

Brown B.M.,Edith Cowan University | Bourgeat P.,Edith Cowan University | Peiffer J.J.,Austin Health | Burnham S.,CSIRO | And 14 more authors.
Neurology | Year: 2014

Objective: To investigate the association between habitual physical activity levels and brain temporal lobe volumes, and the interaction with the brain-derived neurotrophic factor (BDNF) Val66- Met polymorphism. Methods: This study is a cross-sectional analysis of 114 cognitively healthy men and women aged 60 years and older. Brain volumes quantified by MRI were correlated with self-reported physical activity levels. The effect of the interaction between physical activity and the BDNF Val66Met polymorphism on brain structure volumes was assessed. Post hoc analyses were completed to evaluate the influence of the APOE e4 allele on any found associations. Results: The BDNF Val66Met polymorphism interacted with physical activity to be associated with hippocampal (b 5 20.22, p 5 0.02) and temporal lobe (b 5 20.28, p 5 0.003) volumes. In Val/Val homozygotes, higher levels of physical activity were associated with larger hippocampal and temporal lobe volumes, whereas in Met carriers, higher levels of physical activity were associated with smaller temporal lobe volume. Conclusion: The findings from this study support higher physical activity levels in the potential attenuation of age- And disease-related hippocampal and temporal lobe volume loss in Val/Val homozygotes. © 2014 American Academy of Neurology.

Martins I.J.,Edith Cowan University | Martins I.J.,University of Western Australia | Gupta V.,Edith Cowan University | Gupta V.,University of Western Australia | And 6 more authors.
Current Proteomics | Year: 2014

Proteomics has advanced and identified various plasma proteins that may be implicated in lesions in brains from neurodegenerative individuals. Apolipoprotein E and amyloid beta are amongst the many candidate proteins identified in common neurodegenerative disorders with effects by diet and nutriproteomics on the interactions of apo E and amyloid beta. The purpose of this review paper is to specify the role of proteins and lipoproteins and their effects on hepatic amyloid beta clearance that are important to brain amyloidosis. In recent and historical research provided in various research papers the blood brain barrier (BBB) is abnormal in neurodegenerative disease and proteins and oxidized lipids leak across the BBB. The improved scientific understanding of apo E/amyloid beta interactions identifies modulations in protein structure and lipid:protein interactions induced by nutrients and has become important to peripheral amyloid beta metabolism. Hepatic acute phase proteins induced by diet, inflammation and oxidative stress are connected to the pathophysiology of neurotoxic diseases. Oxidative stress induced by high cholesterol diets can cause electrostatic alterations in amyloid oligomers accompanied with alterations in oxidized lipids and acute phase proteins. Recent progress in proteomics with relevance to Alzheimer’s disease has led to the identification of acute phase proteins and include pentraxins that regulate or reduce amyloid beta sizes that are related to membrane permeability and disruption. In this review research papers identify acute phase biomarkers that are involved in the alterations of amyloid beta oligomers in obesity and diabetes with increased BBB permeability and central nervous system disorders. © 2014 Bentham Science Publishers.

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