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The Involvement of Lipids in Alzheimer's Disease

Journal of Genetics and Genomics 2014年第5期41卷 261-274页

作者： Wei Ling Florence Lim Ian James martins ralph nigel martins School of Medical Sciences Edith Cowan University Centre of Excellence in Alzheimer's Disease Research and Care McCusker Foundation for Alzheimer's Disease Research Inc. Suite 22 Hollywood Medical Centre School of Psychiatry and Clinical Neurosciences The University of Western Australia

It has been estimated that Alzheimer＇s disease （AD）, the most common form of dementia, will affect approximately 81 million individuals by 2040. To date, the actual cause and cascade of events in the progression of this disease have not been fully determined. Furthermore, there is currently no definitive blood test or simple diagnostic method for AD. Considerable efforts have been put into proteomic approaches to develop a diagnostic blood test, but to date these efforts have not been successful. More recently, there has been a stronger focus on lipidomic studies in the hope of increasing our understanding of the underlying mechanisms leading to AD and developing an AD blood test. It is well known that the strongest genetic risk factor for AD is the e4 variant of apolipoprotein E （APOE）. Evidence suggests that the ApoE protein, a major lipid transporter, plays a key role in the pathogenesis of AD, and its role in both normal and aberrant lipid metabolism warrants further extensive investigation. Here, we review ApoE-lipid interactions, as well as the roles that lipids may play in the pathogenesis of AD.

关键词： Alzheimer's disease Lipids ApoE Oxysterols Inflammation

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

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Health 2013年第5期5卷 913-920页

作者： Ian James martins Wei Ling Florence Lim Andrea C. Wilson Simon M. Laws ralph nigel martins Centre of Excellence in Alzheimer’s Disease Research and Care School of Medical Sciences Edith Cowan University Joondalup Australia

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.

关键词： Telomere Sirtuin 1 Lifestyle Nutrition Diabetes Obesity Alzheimer’s Disease

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Sirtuin-1 mediates the obesity induced risk of common degenerative diseases: Alzheimer’s disease, coronary artery disease and type 2 diabetes

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Health 2012年第12期4卷 1448-1456页

作者： Ian James martins Andrea. C. Wilson Wei Ling Florence Lim Simon. M. Laws Stephanie. J. Fuller ralph nigel martins Centre of Excellence in Alzheimer’s Disease Research and Care School of Medical Sciences Edith Cowan University Perth Australia McCusker Alzheimer’s Research Foundation Hollywood Medical Centre Perth Australia School of Psychiatry and Clinical Neurosciences The University of Western Australia Perth Australia

Obesity, especially at mid-life, is a major risk factor for atherosclerosis, insulin resistance and the metabolic syndrome, which in turn contribute to coronary artery disease (CAD), Type 2 diabetes and Alzheimer’s disease (AD). The rise in overweight and obesity in all societies is prompting intense research into the causes and effects of the condition. Obesity disrupts many body systems including glucose and lipid metabolism, circadian rhythms and liver function. It also causes or increases inflammation and oxidative stress. Within cells, the endoplasmic reticulum (ER) appears to be particularly susceptible to such metabolic disruption. Sirtuin 1?(Sirt1) and leptin have received attention recently as they are central regulatory factors for the body’s metabolic pathways which interact at particular levels, for example lipid and Abeta metabolism. This mini-review discusses recent findings concerning obesity, lipid metabolism and the role of Sirtuin 1 and how all influence the ER. A greater understanding of obesity and its effects on metabolic control systems of the body are required, to develop pharmacological, dietary and lifestyle changes that will reduce the incidence of CAD, Type 2 diabetes and AD.

关键词： Obesity Sirtuin 1 Alzheimer’s Disease Cardiovascular Disease Diabetes

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