Cognitive Deterioration in Alzheimers Disease - Research Paper Example

? Cognitive Deterioration in Alzheimer’s disease Introduction Alzheimer’s disease (AD) is a devastating disease which takesaway the most imperative aspect of a person – their sense of self (Williams et al., 2010). The disease significantly impacts the patient, family, community, caregivers and society as a whole. AD is a neurodegenerative disease that starts in the temporal lobe leading to memory deficits (Alafuzoff et al., 2008). The pathology soon spreads to other parts of the brain leading to dementia. Dementia is the loss of cognitive abilities in various domains, leading to impairment in activities of daily living and the loss of independence (American Psychiatric Association [DSM-IV-TR], 2000). This paper explores the various aspects of cognitive deterioration in Alzheimer’s disease. It also elaborates on risk factors, and deals with the factors that decrease the risk of cognitive decline in AD. The term cognitive deterioration encompasses a continuum of cognitive changes (Albert et al., 2011). Some of these changes are considered to be with the limits of normal aging. Performance in one or more of the following cognitive domains is used to assess the cognitive deterioration: memory, executive function, orientation, language and praxis. The diagnostic threshold between pathological and normal aging is imprecise. Pathological cognitive decline may range from mild cognitive impairment to full-blown dementia. Each of these terms has multiple subtypes that reflect the construct of multiple etiologies (Albert et al., 2011). Alzheimer’s disease is responsible for more than 50% of all dementia (Alzheimer’s Association, 2013). Age is the major AD risk factor, with the disease prevalence doubling every five years from the age of 65 (Williams et al., 2010). The worldwide prevalence of the disease was estimated at 35.6 million in the year 2010. The number is projected to exceed 65 million by the year 2030, making it a pressing global concern in the field of mental health (Alzheimer’s Association, 2013). Dementia due to AD is associated with an increased burden of co-existing diseases, placement in nursing homes, and an increased mortality (Williams et al., 2010). Caregivers and families often experience financial and emotional stress. According to Alzheimer’s Association (2013), AD accounts for more than 4 % of all the disability-adjusted life years (DALY) in those over 60. In the same report, cognitive impairment is the condition most significantly associated with institutionalization. Framework for Diagnosis The term “dementia” encompasses a group of disorders which result in cognitive deterioration due to damage or death of brain cells. In its definition, dementia leads to a decline in at least 2 of 4 cardinal cognitive functions: (1) memory; (2) capacity to plan, carry out complex tasks and make sound judgment; (3) ability to speak or to understand language; (4) and the ability to interpret and process visual information. The cognitive decline should be severe enough to impair day-to-day life (American Psychiatric Association [DSM-IV-TR], 2000). The typical AD’s cognitive impairment begins with short-term memory loss. Despite these cognitive symptoms, the diagnosis of the disease is that of exclusion. Dementia must be identified by clinical examination and then confirmed by neuropsychological testing. Suspected dementia due to AD should involve multiple, progressive deterioration in cognition in the elderly patient, in the absence of neurological, psychiatric or medical conditions that may account for the deficits. The Diagnostic and Statistical Manual (4th Edition) offers a stepwise diagnosis of the various cognitive deterioration in AD (American Psychiatric Association [DSM-IV-TR], 2000). The first step is the progression in memory loss. The second step is the presence of at least one other cognitive deficit (aphasia, apraxia, agnosia or a disturbance in the executive functions). These cognitive deficits should be severe enough to cause impairment in social or occupational performance, and must represent a decrease from a previous functioning level. In AD, disturbances in executive functioning are common. In the DSM-IV-TR, executive functioning is described as the “ability to think in an abstract manner and to plan, initiate, monitor, and stop complex behavior” (American Psychiatric Association [DSM-IV-TR], 2000). The affected individual has problems coping with new tasks and avoids situations which require the processing of novel and complex information. The tests for executive function may include subtracting serials of 7s from 100, reciting the alphabet, stating as many animals as they can in one minute or counting to 10. Many times, these individuals or their caregivers report problems with the ability to plan daily activities, to work, budget among others. Before the diagnosis of dementia due to AD can be made, various other etiologies should be ruled out. Delirium may cause memory impairment but is short-lived and less stable than dementia. Severe impairment of memory without the presence of other cognitive impairment qualifies as amnestic disorder, but not dementia. Other conditions that should be ruled out and cause dementia include vascular dementia, HIV, stroke and encephalitis. In addition, substance intoxication or withdrawal may lead to dementia. After ruling out all these factors, the dementia of Alzheimer’s type may be considered, as long as the history includes a gradual onset with continuing deterioration (American Psychiatric Association [DSM-IV-TR], 2000). Cognitive Assessment in AD In order to evaluate the cognitive deterioration in AD, it is important to have proper methods of cognitive assessment (Albert et al., 2011). Impairment in episodic memory is one of the earliest cognitive symptoms in AD. There are various memory tests that are useful in identifying early memory impairment. These tests identify those with a high likelihood of progressing to dementia. These tests assess immediate and delayed recall. Therefore, they can determine the retention over delay. World-list learning tests reveal the rate of learning over time, in addition to the maximum amount of information acquired, during the course of the tests. Examples of these tests include the California Verbal Learning test, the Free and Cue selective reminding test and the Rey Auditory verbal learning test. Another measure of episodic memory includes the Wechsler Memory scale which also tests the immediate and delayed recall of non-verbal materials (Albert et al., 2011). Other cognitive domains with specific assessment modalities include: executive functions (such as reasoning, planning, problem-solving and set-shifting); language (such as fluency, naming, comprehension and expressive speech); attentional control (such as divided and simple attention); and visuospatial skills. There are various neuropsychological measures that can be used to assess these cognitive domains. These include the Boston Naming test (language), the Trail Making test (executive function), digit span forward (attention) and figure copying (spatial skills) (Albert et al., 2011). If formal cognitive testing is not possible, cognitive function may be assessed with the use of a variety of informal, simple techniques. The clinician may ask the patient to learn an address (such as John Davies, 33 Market Street, Chicago) and ask the patient to recall it after a delay interval. Nonetheless, it is imperative to note that these informal tests are likely to be insensitive to subtle cognitive impairment (Albert et al., 2011). Brain Changes leading to Cognitive Impairment During autopsy, the Alzheimer’s brain exhibits diffuse changes including atrophy (Alafuzoff et al., 2008). On the outer layer of the brain, the grooves (sulci) are widened, and the folds (gyri) are noticeably shrunken. The brain mass is decreased up to 1/3rd. This is attributed to the loss of synapses, nerve cells and dendrites. The neocortex becomes progressively degenerated. Amyloid deposition in the limbic system (hippocampus, amygdala and entorhinal cortex) leads to increasing impairment in emotional capabilities. The hippocampus and entorhinal cortex work in tandem for memory and learning (Alafuzoff et al., 2008). The entorhinal cortex is responsible for memory. It is the first area to show abnormality, and this is consistent with the fact that memory loss is usually the earliest symptom of AD (Alafuzoff et al., 2008). The amygdala is responsible for emotional screening. As the zone deteriorates, the individual looses the ability to appreciate the emotional importance of new experiences. Within the vicinity of amyloid plaques deposition in the AD brain, chronic inflammation is noticeable. Oxidative stress is also evident in these individuals. Numerous oxidative stress biomarkers are increased in the brain and blood (Gibson & Blass, 2007). Risk Factors for Alzheimer’s disease and Cognitive Decline Findings from clinical and epidemiological studies suggest that multiple behavioral, biological, environmental and social factors contribute to the development or delay of cognitive impairment in AD. Many factors work synergistically to increase the development of cognitive impairment in AD. While some of these factors are non-modifiable, a significant number of them are modifiable. Modification of these factors is possible if the patients are motivated and have professional help. Non-modifiable risk factors include age, gene, mutations and family history. Age is the undisputed risk factor for development of AD. Nonetheless, the increase in geriatric research has led to the concept of successful aging. Drachman (2006) wrote an analysis of AD. The author identified advancing age as the predominant risk factor for the disease and associated cognitive deterioration. From Drachman’s (2006) perspective, the development of AD and cognitive deterioration results from a multiplicity of age-related changes. Recognizing the contribution of these changes will enable care-givers to decrease their burden. Nonetheless, Doidge (2007) argues that even young people also get Alzheimer’s and its cognitive manifestation. Bower (2007) suggests that the brain has powerful adaptability (neuroplasticity). Neuroplasticity protects the individual from cognitive impairment. Bower (2007) undertook a study on rodents. The cage environment was altered to provide various degrees cognitive stimulation. The rodents with more opportunities to exercise their brain (colored toys) and bodies (treadmill) exhibited more neuroplasticity. This was evidenced by new brain dendritic connections, synaptic connections, capillaries and other support tissues. Henceforth, as long as one constantly uses the brain, the onset of cognitive impairment is delayed. All major head injuries can increase the risk of AD and accelerate to the cognitive deterioration (Szczygielski et al., 2005). After some few hours of brain injury, there is an abnormal pattern of amyloid deposition in the brain tissue. Repeated brain injury, even if minor, accelerates amyloid deposition and accelerates cognitive impairment. Sports such as boxing, football and ice hockey facilitate head impacts. According to Szczygielski (2005), boxers who have had more than 10 brain injuries tend to have a poor cognitive outcome. Modifiable risk factors include smoking, hypertension, homocysteine, obesity and type 2 diabetes mellitus (Patterson et al., 2008). Smoking is strongly associated with dementia and cognitive decline. Smokers have twice the risk of being diagnosed with AD. Individuals who are smokers at the time of Alzheimer’s onset tend to die earlier than smokers. The cognitive deterioration in these individuals is accelerated. There is also a dose-dependent effect between disease severity and cigarette pack-years. The more cigarettes the individual smokes, the more the cognitive deterioration (Patterson et al., 2008). Obesity, hypertension and high-cholesterol levels elevate the risk for AD (Patterson et al., 2008). Additionally, cognitive decline is worsened by the presence of these factors. Type 2 diabetes is related to a higher risk of AD. Hyperinsulinemia in Type 2 DM accelerates the functional cognitive decline. Further, insulin resistance has been implicated in the pathogenesis of AD (Patterson et al., 2008). Factors decreasing the risk of cognitive decline Physical Activity Physical activity increases cognitive and brain function. The cortex and hippocampus generate nerve cell precursors throughout their life. Physical exercise increases the mitosis rate in these two zones leading to new nerve growth. On the other hand, lack of physical activity inhibits the differentiation of new precursor cells to functional brain cells (Kramer & Erickson, 2007). A majority of population-based epidemiological studies have found that people who exercise more than 3 times weekly have a lower risk of dementia than those who exercise less. According to Kramer and Erickson (2007), there is a positive correlation between cognition and physical exercise. Cognitively impaired and normal adults derive benefits from increased physical exercise. Physical exercise is greatest for executive function processes. These include working memory, planning, scheduling, multitasking and dealing with distraction. These processes normally tend to decrease with age. According to Etnier et al. (2006), walking (more than 1 hr/day, 3 days a week) increases the gray matter volume in the temporal and frontal cortex. Aerobic exercise enhances neurogenesis by elevating growth factors. Additionally, it also brain cell survival and cell proliferation. Exercise has profound health benefits. By increasing blood flow and circulation, it decreases the risk of diabetes, stroke, heart attack, all of which are linked to accelerated cognitive deterioration (Etnier et al., 2006). Mental Exercises Mental exercise entails training the brain. As with physical exercise, experiments with animals have demonstrated that mental exercise supports neurogenesis Willis et al. (2006), Stress and the lack of mental exercise allow the stem cell progeny to die off. According to the concept of neuroplasticity noted above, it is possible to remold and rebuild the brain via “brain training” (Willis et al., 2006). This is an interesting area in the field of brain health management. Brain fitness or neurobics involves mental exercise with interactive tests, online courses, video games, DVDs among other media. Willis et al. (2006) conducted a single blind randomized control trial, which divided the participants into four groups – reasoning, memory, processing speed and the Controls. Each group was undertaken through a 10 week cognitive training, then a four session booster training. At 5th year of follow-up, the three actively trained groups (memory, reasoning and processing speed) exhibited significant cognitive improvements when compared to the controls. Outcomes from such brain training imply that the human brain is resilient; hence, consistent with the animal study findings. The brain is capable of rebuilding lost circuits. This is an imperative field in halting or preventing cognitive deterioration in AD. Dietary and Nutritional Factors A high intake of omega-3-fatty acids is linked to lower risk of developing dementia, or the progression. Better omega-3-fatty acid status correlates with slower cognitive deterioration over time. Fish contain high amounts of omega-3-fatty acids (Freund-Levi et al., 2008). Consumption of one fish meal weekly significantly decreased the risk of AD compared to individuals who never/rarely eat fish. Additionally, omega-3-fatty acids further protect from diabetes, cardiovascular dysfunction and systemic inflammation, all of which are risk factors for AD development. Cold-water fish are the best sources of omega-3-fatty acids. Other sources include supplements, eggs and other staple foodstuffs. Omega-6 essential fatty acids also enhance cognitive function (Freund-Levi et al., 2008). When vitamin E is taken at a high daily intake, it delays cognitive decline progression. Increasing evidence suggests that nutrients regulate gene activities. Vitamin E deficiency may have a strong impact on hippocampus gene expression (Rota et al., 2005). Hippocampus is a key brain area afflicted by AD. Vitamin E also operates with endogenous antioxidant enzymes and other antioxidants. Alzheimer patients tend to have a lower level of Vitamin E. Nonetheless, this might be attributed to the poor eating habit linked to the disease. Other vitamins that have been shown to have neuroprotective actions include folic acid, vitamin B12, and vitamin B1 (thiamine) (Gibson & Blass, 2007). Deficiency of all these vitamins is noted in many Alzheimer patients. Thiamine is imperative for glucose metabolism. It is known to decline early in the disease. Thiamine deficiency may lead to irreversible cognitive impairment. There is a protective association between intake of high vegetable amounts and lower rates of cognitive deterioration. Trace elements have also been shown to enhance cognitive function. These include selenium, copper, iron and zinc. Nonetheless, a higher intake of these elements may negate their benefits. A high intake of copper is associated with a greater cognitive decline, especially in individuals consuming a diet high in trans-fats and saturated fats (Gibson & Blass, 2007). Conclusion Alzheimer’s disease is a devastating illness. Cognitive function is impaired very early in the course of the disease. Memory deficit is one of the earliest symptoms noted. Eventually, executive functioning including attention control, inhibition and working memory will be affected. There are various factors associated with the risk of cognitive deterioration or acceleration of the same. These include modifiable and non-modifiable factors. Non-modifiable risk factors include age, mutations, family history and genes. Modifiable risk factors include smoking, hypertension, homocysteine, obesity and type 2 diabetes Mellitus. Trauma to the head also impacts negatively on cognitive function. There are various factors and intervention that improve or maintain cognitive function or ability in Alzheimer’s disease. Physical and mental exercise foster proper brain functioning and prevent cognitive deterioration. Mental health is essentially imperative in regeneration of new neuronal circuitry. When administered by properly trained staff, the brain function is maintained or restored to a significant level. Brain training, in addition to mass screening of cognitive function and performance, is feasible with the use of psychometrics. Additionally, there are various nutritional factors that enhance cognitive function. These include unsaturated fatty acids, various vitamins and trace-elements. A combination of these factors may facilitate the development of an integrative primary prevention for the at risk population. Reference List American Psychiatric Association. (2000). Diagnostic and statistical manual of mental disorders. DSM-IV TR. Washington, DC: Author. 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