Alzheimer's disease (AD) is the leading cause of dementia and the most common neurodegenerative disease in the elderly. Furthermore, AD has provided the most positive indication to support the fact that inflammation contributes to neurodegenerative disease. The exact etiology of AD is unknown, but environmental and genetic factors are thought to contribute, such as advancing age, family history, presence of chronic diseases such as cardiovascular disease (CVD) and diabetes, and poor diet and lifestyle. It is hypothesised that early prevention or management of inflammation could delay the onset or reduce the symptoms of AD. Normal physiological changes to the brain with ageing include depletion of long chain omega-3 fatty acids and brains of AD patients have lower docosahexaenoic acid (DHA) levels. DHA supplementation can reduce markers of inflammation. This review specifically focusses on the evidence in humans from epidemiological, dietary intervention, and supplementation studies, which supports the role of long chain omega-3 fatty acids in the prevention or delay of cognitive decline in AD in its early stages. Longer term trials with long chain omega-3 supplementation in early stage AD are warranted. We also highlight the importance of overall quality and composition of the diet to protect against AD and dementia.

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The interest in the cardioprotective effects of long chain omega-3 polyunsaturated fatty acids (LCn3) was largely influenced by the low rates of cardiovascular disease (CVD) amongst the Inuits of Greenland who consumed a high marine fat diet rich in LCn3s. This finding stimulated years of epidemiological and clinical studies investigating the cardioprotective effects of LCn3s, thought to be primarily mediated through anti-inflammatory (and antiaggregatory) prostaglandins that protect the vascular wall from pro-inflammatory effects of metabolic stress precipitated by poor diet and lifestyle. Although the original hypothesis of the link between LCn3s and CVD protection was based on a high LCn3 containing diet (namely a high marine fat diet) the majority of clinical trials since have focussed on EPA and DHA supplementation, and results of repeated meta-analyses have not shown conclusive evidence in support of their beneficial health effects. In this review we focus on the controversies that surround the efficacy of LCn3s in cardiovascular and other chronic diseases and present emerging areas of research for novel applications. We will examine factors that can impact on the efficacy of LCn3s such as source (plant vs marine vs supplements (algal vs marine)), stability of product, dose, trial duration, ratio of EPA:DHA, and ratio of LCn6:LCn3 fatty acids in the diet.

Accumulating evidence indicates that hyper-glycaemia is deleterious to brain function, in particular to the hippocampus. It is thought this hippocampal dysfunction may contribute to hyperglycaemia related cognitive impairment, such as that which manifests with diabetes. In the present study, we investigated the effects of diabetes-related hyperglycaemia on hippocampal gene expression, in order to identify potential mechanisms that might be associated with the cognitive dysfunction that develops with diabetes mellitus. Genome-wide gene expression profiling was carried out on the hippocampi from streptozotocin (STZ)-induced diabetic mice, and from vehicle treated control mice. Genes of interest that satisfied expression fold-change and statistical criteria, and that were considered to be potentially associated with cognitive function, were further tested by real time, quantitative polymerase chain reaction (qPCR) analysis. We found that STZ-induced diabetes resulted in decreased hippocampal expression of genes involved in epigenetic regulation and synaptic plasticity, for example, histone deacetylases and glycogen synthase kinase 3 beta (HDACs and GSK3β). We also found increased expression of genes involved in signalling cascades related to cell growth, cell survival and energy metabolism, such as neurotropic tyrosine kinase receptor type 2, apolipoprotein E, and protein tyrosine phosphatase receptor type (Ntrk2, APOE, PTPRT). To our knowledge this is the first study to demonstrate a gene expression profile implicating epigenetic modifications and alterations of synaptic plasticity associated genes in diabetes mellitus. The present study will improve our understanding of the neural mechanisms that might underpin diabetes-related cognitive dysfunction.

Self-medication practices of type 2 diabetes in India include the use of both traditional and western medications. It is important to understand the factors influencing self-medication. A total of 3257 studies were screened and nine studies (six quantitative and three qualitative) were included. The Hawker tool and Joanna Briggs Institute Critical Appraisal tool were used to assess the quality of studies. The findings of the quantitative studies were descriptively analysed while thematic analysis was performed to identify key themes from the qualitative studies. The analysis indicated that participants had greater trust in traditional medications regardless of their socioeconomic and/or educational backgrounds as these were often recommended by friends and family members. Low cost, ease of availability and perceived lower side effects of traditional medications were some of the factors contributing to greater trust. It is suggested that ongoing management of type 2 diabetes requires stringent policies and regulations in the dispensing of traditional and western medications. Continual education to inform people on the use of self-medications and its possible adverse effects is also required.