Alzheimer Disease, Dementia - Essay Example

? Introduction Dementia delineates an umbrella term embodying diversity of diseases and conditions that stem from the dying of nerve cells within the brain or when they fail to function properly. The death or breakdown of the nerve cells (neurons) yields changes within one’s memory, behaviour, and capability to think properly. Alzheimer’s disease is the predominant form of dementia and is estimated to result in 60-80% of registered cases (Alzheimer’s Association, 2012, p. 4). The exact cause of AD is unknown; however, the majority of experts agree that AD, just as other chronic illnesses, stems from multiple factors rather than a solitary cause. In AD, information transfer at synapses is unsuccessful as the number of synapses reduces and neurons ultimately die. The most dominant risk factor of AD entails advancing age with other risk factors detailing family history, Apolipoprotein E-?4, mild cognitive impairment, cardiovascular disease risk factors, head trauma and traumatic brain injury, and diet. Statistics indicate that approximately one in eight older Americans manifests Alzheimer’s disease (13%). Nearly 50% of all persons aged 85 years and above have AD. It is anticipated that the number of Americans with Alzheimer’s disease plus other dementias will increase each year as the aging U.S. population averaging around 65 years increases. Similarly, the dementia incidence within developing countries has increased considerably in line with an ageing population (Kalaria et al., 2008, p. 812). Alzheimer’s disease accounts for close to 60% whereas vascular dementia relates to 30% of the incidence. Vascular factors such as type 2 diabetes and hypertension are highly probable to enhance the burden of dementia. Diet and lifestyle have been shown to impact the risk of AD with studies implying that midlife history of disorders that influence the vascular system such as type 2 diabetes, obesity, and hypertension, enhance the risk of dementia inclusive of Alzheimer’s disease (AD) (Luchsinger, 2007, p. 119). Increasing trends manifested in demographic transition and rapid urbanization within the majority of developing countries is predicted to lead to dramatic lifestyle changes and, consequently, an enhanced incidence of AD. Risk Factors of Alzheimer's Disease Scientists have highlighted several factors that appear to play a significant role in the development of AD; however, no classic causes have been found to solely cause the complex disorder. Scientists cite age as the most significant factor that causes AD, in addition to other factors such as genetics, environment, and lifestyle. Age Increasing age can be delineated as the greatest known risk factor of AD. Alzheimer’s is not part of usual aging, but the risk of AD amplifies as one grows older. After an individual attains the age of 65, the risk of developing AD doubles about every five years whereby close to half of those aged 85 have AD. Family History and Genetics Late onset Alzheimer’s disease (AD) represents a multifactorial and heterogeneous disorder with significant risk factors encompassing advanced age, incidence of apolipoprotein E (APOE4) allele, and familial history regarding AD. The predisposition to developing AD appears to be fairly higher in cases where a first degree relative has the disease. Scientists have highlighted rare changes (mutations) in three genes that ensure that an individual who inherits them will highly likely develop AD. Nevertheless, these mutations account for less than 5% of AD. The chief risk protein gene that has been highlighted so far to predispose the onset of AD encompasses apolipoprotein ?4 (APOE-?4) (Messier, 2003, p. 941). It is estimated that close to one in four Americans manifests ApoE4, while one in twenty manifests ApoE2 (Martins et al., 2006). While heredity of the ApoE4 enhances the predisposition to developing AD, ApoE2 considerably safeguards against it. Early manifestation of Alzheimer does remain largely inherited, exceptional form of the disease affecting less that 10% of patients. This stems from three gene mutations on chromosomes 1, 14, and 21 (Grant et al., 2002, p. 179). Lifestyle There is no lifestyle factor that can be conclusively delineated to cause one’s risk of Alzheimer’s disease. Nevertheless, some evidence suggests that some of the factors that predispose individuals to heart disease may also enhance the probability that the individual will develop AD (Rocchi et al., 2009, p. 224). These factors encompass aspects such as high cholesterol, high blood pressure, poorly managed diabetes, and lack of exercise (Solfrizzi et al., 2011, p. 677). These risk factors are also attached to vascular dementia, a form of cognitive decline orchestrated by damaged blood vessels within the brain. Cardiovascular Disease High blood pressure may lead to the damaging of blood vessels within the brain, disrupting regions that are critical in memory, verbal skills, and decision-making. This could add to the progression of the disease. Besides, high cholesterol may hamper the ability of blood to remove protein from the brain. Type 2 Diabetes Type 2 diabetes (the most common) details a condition in which the body experiences excessive blood glucose. This emanates from a deficiency in insulin, which is a hormone that is naturally produced within the body to signal the liver, body muscles, and body fat to absorb glucose from the blood (Craft, 2005, p. 65). Studies indicate that diabetes dramatically enhances an individual risk of developing AD or other forms of dementia (Reger et. al., 2008, p. 323). The inefficiency registered yields in the production of enhanced levels of insulin and blood sugar that may damage the brain and contribute to the progression of Alzheimer’s. Experimental evidence implies that anomalies in insulin metabolism during diabetic conditions mechanistically impact the onset of AD through their control over the synthesis and degradation of amyloidogenic A? peptides. Furthermore, increased amounts of insulin in circulation during diabetic conditions may also aggravate amyloid accumulation by automatically competing with A? for the insulin-degrading enzyme (Craft, 2007, p. 147; Cao et al., 2007, p. 36275). Inflammation Inflammation details a natural but sometimes damaging healing bodily function whereby immune cells rid themselves of dead cells plus other waste products. As protein plaques establish inflammation results, it is alleged that this process may be damaging and cause Alzheimer’s (Misiak, Leszek, & Kienjna, 2012, p. 144). How Dietary Factors and Metabolic Components Are relevant to Alzheimer's Disease Dietary intake of whole grains, low in sugar, vegetables, and fruits may minimize the incidences of the majority of chronic diseases, and researchers continue to probe whether the dietary modifications are applicable to AD. Scientists advise that individuals should follow dietary advice critical to lowering the risk of metabolic disorders and cardiovascular diseases, such as a diet low in foods with added sugars. How Obesity Is Related to Alzheimer's Disease Obesity hastens cognitive decline and Alzheimer’s disease progression whereby obesity increases the risk of heart disease, stroke, diabetes, and dementia in direct relation to obesity measures (Kaderali, Ratcliffe, & Dale 2009, p. 445). Scientists have identified that changes in metabolic factors such as blood sugar, cholesterol, and enhanced blood pressure plus other metabolic factors emanating from obesity, make middle-aged and older adults experience a speedy decline in cognitive skills such as thinking and memory (Lindsay et al., 2002, p. 445). Known metabolic abnormality risk factors encompass aspects such as diabetes, cardiovascular disease, and dementia. Much epidemiological proof points out that type 2 diabetes is linked to two- to threefold augmentation in comparative threat to AD, independent of the risk of vascular dementia. High calories intake and consumption of diets rich in sugar and refined flour are significant sources of health concerns, along with sedentary lifestyles, as they have been associated with enhanced relative risk of AD (Profenno, Porsteinsson, & Fraone, 2010, p. 505). The unhealthy lifestyles have increased the incidence of obesity and modified insulin receptor (IR) signalling owing to the hyperglycaemic condition (IR insensitivity). Obesity has received a significant amount of attention as it is labelled a risk factor for AD (Craft, 2007, p. 147). In fact, mounting evidence implies a probable linkage between obesity in middle age and predisposition to dementia later in life. For instance, obese participants (with a BMI greater than or equal to 30 had a 35% enhanced risk of dementia relative to those of normal weight (BMI ranging from 18.6 to 24.9). The study concluded that obesity during middle age enhanced the risk of future dementia autonomously of comorbid conditions. Balakrishnan et al. (2005, p. 269) probed the linkage between plasma A? levels, fat mass, and BMI whereby they established that certain molecular indexes that have been implicated in inflammation processes, hyperglycaemic conditions in Type 2 diabetes, and cardiovascular disorders – which, in turn, are significant risk factors for AD – add to the linkage between BMI/fat mass and plasma A? content (Fewlass et al., 2004, p. 1870). The peptide hormone that is secreted by adipose tissue manifests a broad range of both central and peripheral actions. Chronic administration of leptin to AD-transgenic minimized the brain A? load implying its therapeutic potential in AD (Sami, Dominguez, & Buyse, 2006, p. 271). The Role of Metabolic Disorders in Alzheimer’s Disease The metabolic syndrome is widely known for its intensification role in several diseases, especially cardiovascular disorders. Recent evidence suggests that the metabolic syndrome is a significant risk factor for AD dementia. The metabolic syndrome refers to a group of risk factors that enhance the risk of heart disease plus other health problems such as stroke and diabetes (Haan, 2006, p. 159). Unhealthy lifestyle choices yield to rising incidences of obesity and hypertension. A number of research findings reinforce the hypothesis that calorie intake, in addition to other non-genetic factors, can contribute to the risk of clinical dementia. Relationship Between Cholesterol and Alzheimer's Disease High cholesterol levels are significantly related to brain plaques that are linked to Alzheimer’s disease. Plaques tangled within the brain are regarded as a trademark for Alzheimer’s disease (Sjogren & Blennow, 2005, p. 85). Plaques represent an accumulation of a type of protein known as amyloid that manifests between nerve cells. Individuals with high cholesterol levels usually manifest comparatively a higher density of plaques relative to those with ordinary or decreased cholesterol levels (Shobab, Hsiung, & Feldman, 2006, p. 841). Statistics indicate that nearly 86% of people with high cholesterol manifest brain plaques compared to only 62% of people with low cholesterol levels. Studies have shown that some cholesterol reducing drugs minimize the risk of AD within individuals (Watson & Craft, 2004, p. 97). How Glucose Is Connected to Alzheimer's Disease Special proteins, glucose transporters, aid in passing glucose from the outside to the inside of cells. GLUT-1 is manifested within erythrocyte and the endothelial cells that line blood vessels. GLUT-3 is manifested within neurons whereby GLUT-4 is established within fat and muscle cells (Solomon, 2008, p. 89). In both type 1 and type 2 diabetes, the enhanced level of glucose within the blood can inflict damage to organs such as the heart and kidneys. The growing body of evidence suggesting that AD is a metabolic disease has made some doctors label the disease as “type 3 diabetes” (Monte & Wands, 2008, p. 1101) Diabetes signifies either impairment of body’s capability to yield insulin or some form of inability in glucose-absorbing organs and tissues to obtain and act on the given insulin signals. Role of Insulin in the Brain and Its Connection to AD The metabolic rate is influenced by many factors such as age, body size, weight gain, gender, body consumption, hereditary, hormones, psychological state, and temperature. The human metabolism is also influenced by aspects such as eating habits. Individuals with diabetes are at an enhanced risk of Alzheimer’s disease with strong evidence suggesting that individuals with high insulin levels are already on the road to Alzheimer’s disease (Craft, 2009, p. 300). As the body becomes overweight, it becomes increasingly resistant to the blood sugar lowering impacts of insulin. To overcome the insulin resistance, the body keeps generating more insulin, which escalates the sequence of insulin resistance. Enhanced insulin levels are known to yield inflammation of blood vessels, which, in turn, may lead to insulin caused brain inflammation and consequent amyloid elevations (Simons et al., 2001, p. 1089). Around 2% of the human resting metabolic rate is utilized to power the brain, which means that the brain requires more rest compared to all muscles within the body, kidneys, and the heart combined. Energy used by the brain should be supplied by a steady source of glucose since limited stored energy in the form of glycogen exists. In the event that glucose levels within the blood drop too low, neurons will ultimately stop functioning whereby brain damage occurs. Insulin resistance is highly linked to the degenerative spiral witnessed in AD, especially in glucose metabolism within the brain. How Improving Metabolic Health Prevents and Delays the Onset of Alzheimer’s Disease Recent studies reinforce the hypothesis that the calorie intake, in addition to other non-genetic factors, plays a critical role in enhancing the relative risk of AD clinical dementia. While there is ample evidence suggesting that high calorie promotes AD neuropathology, recent experimental evidence indicates that calorie restriction, mainly through reduced carbohydrate intake, can protect against AD (Seneff, Wainwright, & Mascitelli, 2011, p. 134). This evidence aligns, in part, with present epidemiological studies implying that obesity and diabetes are linked to more than fourfold enhanced risk of developing AD (Luchsinger & Mayeux, 2004, p. 579). The preventative impacts of calorie minimization on the etiology of mild cognitive impairment are reinforced by the potential neuroprotective function for calorie reduction in neurodegeneration. Although these studies imply that alterations in dietary lifestyles such as minimizing calories intake might positively influence AD, it is essential to note that malnutrition remains a significant challenge among the elderly. Thus, dietary recommendations in AD should be given as per the needs of such comorbidities such as type 2 and cardiovascular diseases. Since obesity-Alzheimer’s link has already been established, the reasonable way to minimize the predisposition and delay the onset is via a whole diet approach. The dietary lifestyles should be geared towards preventing metabolic syndrome and ultimately AD (Pasinetti & Eberstein, 2008, p. 1503). The dietary changes should promote whole foods and discourage consumption of refined and extensively processed foods. This is geared towards minimizing exposure to added sugars, refined grains that are not nutritionally beneficial, and manufactured trans fat (Kamphuis & Scheltens, 2010, p. 765). Lifestyle changes may impact positively AD as well as other chronic health conditions such as obesity by normalizing weight, enhancing the constituents of the metabolic syndrome and treating or preventing diabetes and cardiovascular disease. Mediterranean diet has proved beneficial to treating AD owing to its antioxidant plus its anti-inflammatory components such as omega-3 fatty acids (Scarmeas, Stern, Tang, & Mayeux, 2006, p. 912). Fruit and vegetable intake has been linked to enhanced cognitive performance among the elderly. As such, the consumption of fruits and vegetables has been closely connected to decreased incidence of dementia. However, alcohol use and cognitive function among the elderly has delivered inconsistent results. Age-related changes within the nutritional status can play a significant role in brain functioning (Quefurth & LaFerla, 2010, p. 929). Conclusion Alzheimer’s disease is an intricate disorder for which there is no exact known cure or prevention. Some research has produced hope that it may be possible to delay the progression of Alzheimer’s disease, its symptoms or generally prevent it from occurring. Although there is increasing evidence supporting the benefits of some interventions such as cardiovascular risk reduction and physical activity, preventing or postponing the onset of Alzheimer’s disease and hindering its progression would yield to a consequent enhancement of health status and quality of life at an old age. Some of the steps that individuals can adopt in order to lower their risk of developing AD encompass modifying known risk factors of dementia, namely: diabetes, midlife hypertension, smoking, midlife hypertension, depression, physical inactivity, and inadequacy of mental stimulation. These include actions such as controlling diabetes, lowering high blood pressure as well as high cholesterol levels, eating a healthy diet, physical exercise, and engaging in mind stimulating activities. 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