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Whilst the links between a healthy diet and healthy heart are firmly established and well documented, the relationship between diet and brain health is less well understood. Emerging research is ensuring however, that the maxim of ‘what is good for your heart, is also good for your brain’ is gaining momentum. Nutritional status and dietary habits have long been known to influence risk of cardiovascular disease (CVD) and type 2 diabetes mellitus (T2D), and they are now materialising as key factors influencing Alzheimer's disease (AD) risk. This is compounded by the fact that both CVD and T2D are themselves risk factors for AD, and also by the fact that AD is an age‐related condition, and ageing is accompanied by an overall decline in digestive function, absorptive capabilities, and the assimilation of nutrients. Therefore, understanding the effect of macro‐ and micronutrients on neuronal biochemistry and AD pathology will provide opportunities for dietary manipulation to promote neuronal resistance to insults and reduce brain injury. This chapter discusses some of the key nutrients involved both directly in neuronal biochemistry, and indirectly by influencing peripheral metabolism, which in turn can modulate AD pathology.

Alzheimer’s disease (AD) is a degenerative brain disorder and is the most common form of dementia. Minimally invasive approaches are required that combine biomarkers to identify individuals who are at risk of developing mild cognitive impairment (MCI) and AD, to appropriately target clinical trials for therapeutic discovery as well as lifestyle strategies aimed at prevention. Buccal mucosa cells from the Australian Imaging, Biomarkers and Lifestyle Flagship Study of Ageing cohort (n=60) were investigated for cytological markers that could be used to identify both MCI and AD individuals. Visual scoring of the buccal cytome demonstrated a significantly lower frequency of basal and karyorrhectic cells in the MCI group compared with controls. A high content, automated assay was developed using laser scanning cytometry to simultaneously measure cell types, nuclear DNA content and aneuploidy, neutral lipid content, putative Tau and amyloid-β (Aβ) in buccal cells. DNA content, aneuploidy, neutral lipids and Tau were similar in all groups. However, there was significantly lower Tau protein in both basal and karyolytic buccal cell types compared with differentiated buccal cells. Aβ, as measured by frequency of cells containing Aβ signal, as well as area and integral of Aβ signal, was significantly higher in the AD group compared with the control group. Buccal cell Aβ was correlated with mini-mental state examination (MMSE) scores (r = -0.436, P=0.001) and several blood-based biomarkers. Combining newly identified biomarkers from buccal cells with those already established may offer a potential route for more specific biomarker panels which may substantially increase the likelihood of better predictive markers for earlier diagnosis of AD.

Alzheimer's disease (AD), the most common form of dementia, is a chronic, progressive neurodegenerative disease that manifests clinically as a slow global decline in cognitive function, including deterioration of memory, reasoning, abstraction, language and emotional stability, culminating in a patient with end-stage disease, totally dependent on custodial care. With a global ageing population, it is predicted that there will be a marked increase in the number of people diagnosed with AD in the coming decades, making this a significant challenge to socio-economic policy and aged care. Global estimates put a direct cost for treating and caring for people with dementia at $US604 billion, an estimate that is expected to increase markedly. According to recent global statistics, there are 35·6 million dementia sufferers, the number of which is predicted to double every 20 years, unless strategies are implemented to reduce this burden. Currently, there is no cure for AD; while current therapies may temporarily ameliorate symptoms, death usually occurs approximately 8 years after diagnosis. A greater understanding of AD pathophysiology is paramount, and attention is now being directed to the discovery of biomarkers that may not only facilitate pre-symptomatic diagnosis, but also provide an insight into aberrant biochemical pathways that may reveal potential therapeutic targets, including nutritional ones. AD pathogenesis develops over many years before clinical symptoms appear, providing the opportunity to develop therapy that could slow or stop disease progression well before any clinical manifestation develops.

Alzheimer's disease (AD), the most common form of dementia, is a chronic, progressive neurodegenerative disease that manifests clinically as a slow global decline in cognitive function, including deterioration of memory, reasoning, abstraction, language and emotional stability, culminating in a patient with end-stage disease, totally dependent on custodial care. With a global ageing population, it is predicted that there will be a marked increase in the number of people diagnosed with AD in the coming decades, making this a significant challenge to socio-economic policy and aged care. Global estimates put a direct cost for treating and caring for people with dementia at $US604 billion, an estimate that is expected to increase markedly. According to recent global statistics, there are 35·6 million dementia sufferers, the number of which is predicted to double every 20 years, unless strategies are implemented to reduce this burden. Currently, there is no cure for AD; while current therapies may temporarily ameliorate symptoms, death usually occurs approximately 8 years after diagnosis. A greater understanding of AD pathophysiology is paramount, and attention is now being directed to the discovery of biomarkers that may not only facilitate pre-symptomatic diagnosis, but also provide an insight into aberrant biochemical pathways that may reveal potential therapeutic targets, including nutritional ones. AD pathogenesis develops over many years before clinical symptoms appear, providing the opportunity to develop therapy that could slow or stop disease progression well before any clinical manifestation develops.

Molecular mechanisms involved with neuroendocrine diseases such as obesity and diabetes are closely linked to insulinresistance and require attention since metabolic dysfunction has also been associated with neurodegeneration. The global increase in these chronic diseases supports a role for lipids, such as ceramide and its metabolites in the pathogenesis ofthese diseases. The link between the ceramide and its pathogenesis of diabetes has been an important discovery that may assistwith the role of ceramide in the pathogenesis of Alzheimer’s disease (AD) also referred to as Type 3 diabetes. Lipids such as cholesterol and ceramide have been connected to processing of the amyloid precursor protein with generation or regulationof beta-amyloid production that is central to the amyloid hypothesis in AD. The cholesterol-ceramide connection has beenpreviously linked with aging and AD. Lipidomic analysis using mass spectrometry of fasting plasma from an ageing cohort (AIBL) that includes mild cognitively impaired individuals, cognitively healthy controls and AD patients at baseline havebeen provided in this study. The plasma lipid ceramide was elevated in AD patients and this study provides potential for early therapeutic targets that reduce ceramide levels to manage hypercholesterolemia and insulin resistance in both diabetes and AD.

Molecular mechanisms involved with neuroendocrine diseases such as obesity and diabetes are closely linked to insulinresistance and require attention since metabolic dysfunction has also been associated with neurodegeneration. The global increase in these chronic diseases supports a role for lipids, such as ceramide and its metabolites in the pathogenesis ofthese diseases. The link between the ceramide and its pathogenesis of diabetes has been an important discovery that may assistwith the role of ceramide in the pathogenesis of Alzheimer’s disease (AD) also referred to as Type 3 diabetes. Lipids such as cholesterol and ceramide have been connected to processing of the amyloid precursor protein with generation or regulationof beta-amyloid production that is central to the amyloid hypothesis in AD. The cholesterol-ceramide connection has beenpreviously linked with aging and AD. Lipidomic analysis using mass spectrometry of fasting plasma from an ageing cohort (AIBL) that includes mild cognitively impaired individuals, cognitively healthy controls and AD patients at baseline havebeen provided in this study. The plasma lipid ceramide was elevated in AD patients and this study provides potential for early therapeutic targets that reduce ceramide levels to manage hypercholesterolemia and insulin resistance in both diabetes and AD.

Healthy eating habits are important for good health, and eating the right foods can reduce the risk of developing nutrition-related conditions such as diabetes, heart disease and some forms of cancer. Diet also plays an important part in the prevention of Alzheimer’s disease, and can improve quality of life for people with Alzheimer’s disease. This chapter focuses on the relationship between diet and Alzheimer’s disease, and how you can eat your way to a healthier life. We will also show how diet can help to prevent or delay the onset of Alzheimer’s disease, with tips about foods that can help maintain good brain health.

Background A novel IL4RA polymorphism, Ala57Thr, was identified in Greenlander Inuit. Objective We sought to determine whether the novel Thr57 allele is population specific and to assess the associations of Ala57Thr and Ile50Val with atopy in 2 Inuit populations. Methods Ala57Thr and Ile50Val were genotyped in 651 Inuit living in Denmark, 1295 Inuit living in Greenland, and 1329 individuals from 7 populations from widely differing global locations. In Inuit the polymorphisms were evaluated for associations with atopy, rhinitis, asthma, and pulmonary function. Results Thr57 was in linkage disequilibrium with Ile50 (D′ = 1, r2 = 0.13) and was common (33%) in the Inuit but rare (<0.6%) in all other populations. In Inuit living in Denmark, the Thr57 allele (in a dose-dependent manner) and the Ile50/Thr57 haplotype were associated with lower risk of atopy (Plinear = .003 and P = .034, respectively), with similar trends observed for atopic rhinitis and atopic asthma. In Inuit living in Greenland, Thr57 was not associated with atopy or atopic diseases, but Ile50 was weakly associated with lower risk of atopy. Conclusion The novel IL4RA Ala57Thr was common in and population specific to Greenlander Inuit, with Thr57 associated with a lower risk of atopy in those living in Denmark. Hence a full investigation of genotype-phenotype relationships in a given population can only be achieved if each gene is screened for novel polymorphisms in that population. Clinical implications Clinical risk attributable to variations in a gene in an ethnic group requires that all variations of the gene are known for that group.

Background A novel IL4RA polymorphism, Ala57Thr, was identified in Greenlander Inuit. Objective We sought to determine whether the novel Thr57 allele is population specific and to assess the associations of Ala57Thr and Ile50Val with atopy in 2 Inuit populations. Methods Ala57Thr and Ile50Val were genotyped in 651 Inuit living in Denmark, 1295 Inuit living in Greenland, and 1329 individuals from 7 populations from widely differing global locations. In Inuit the polymorphisms were evaluated for associations with atopy, rhinitis, asthma, and pulmonary function. Results Thr57 was in linkage disequilibrium with Ile50 (D′ = 1, r2 = 0.13) and was common (33%) in the Inuit but rare (<0.6%) in all other populations. In Inuit living in Denmark, the Thr57 allele (in a dose-dependent manner) and the Ile50/Thr57 haplotype were associated with lower risk of atopy (Plinear = .003 and P = .034, respectively), with similar trends observed for atopic rhinitis and atopic asthma. In Inuit living in Greenland, Thr57 was not associated with atopy or atopic diseases, but Ile50 was weakly associated with lower risk of atopy. Conclusion The novel IL4RA Ala57Thr was common in and population specific to Greenlander Inuit, with Thr57 associated with a lower risk of atopy in those living in Denmark. Hence a full investigation of genotype-phenotype relationships in a given population can only be achieved if each gene is screened for novel polymorphisms in that population. Clinical implications Clinical risk attributable to variations in a gene in an ethnic group requires that all variations of the gene are known for that group.

This article provides an overview of the extent of casualisation of the nursing workforce in Australia, focusing on the impact for those managing the system. The implications for nurse managers in particular are considerable in an industry where service demand is difficult to control and where individual nurses are thought to be increasingly choosing to work casually. While little is known of the reasons behind nurses exercising their preference for casual work arrangements, some reasons postulated include visa status (overseas trained nurses on holiday/working visas); permanent employees taking on additional shifts to increase their income levels; and those who elect to work under casual contracts for lifestyle reasons. Unknown is the demography of the casual nursing workforce, how these groups are distributed within the workforce, and how many contracts of employment they have across the health service--either through privately managed nursing agencies or hospital managed casual pools. A more detailed knowledge of the forces driving the decisions of this group is essential if health care organisations are to equip themselves to manage this changing workforce and maintain a standard of patient care that is acceptable to the community.

This article provides an overview of the extent of casualisation of the nursing workforce in Australia, focusing on the impact for those managing the system. The implications for nurse managers in particular are considerable in an industry where service demand is difficult to control and where individual nurses are thought to be increasingly choosing to work casually. While little is known of the reasons behind nurses exercising their preference for casual work arrangements, some reasons postulated include visa status (overseas trained nurses on holiday/working visas); permanent employees taking on additional shifts to increase their income levels; and those who elect to work under casual contracts for lifestyle reasons. Unknown is the demography of the casual nursing workforce, how these groups are distributed within the workforce, and how many contracts of employment they have across the health service--either through privately managed nursing agencies or hospital managed casual pools. A more detailed knowledge of the forces driving the decisions of this group is essential if health care organisations are to equip themselves to manage this changing workforce and maintain a standard of patient care that is acceptable to the community.

5th World Congress on Diabetes and Metabolism, held at Embassy Suites, Las Vegas, United States of America, 3-5 November 2014.Original poster Available here