Pathological Processes in the CNS and the Rest of the Body - Essay Example

Pathological processes in the CNS and the rest of the body are similar. This paper will focus on pathological processes between Alzheimer’s disease and type 2 diabetes. These diseases are known to be degenerative and metabolic disorders. Many studies have been conducted show that there is a strong connection between type 2 diabetes and development of Alzheimer’s disease. Researchers have identified several pathological features that are common in both type 2 diabetes and Alzheimer’s patients. Some common features of these two diseases include inflammation, insulin resistance and dyslipidemia. Abnormal insulin signaling is not only involved at the glucose level but also at numerous degenerative processes. Another common feature between these two diseases is that their prevalence increases as age advances (Abbas, et al., 2009). This paper will review the common inflammatory and pathological processes in the CNS and the rest of the body. Alzheimer Disease Alzheimer’s disease is the most common form of dementia among older people. It is associated with the loss of cognitive functions like thinking, remembering and reasoning to an extent where it interferes with the patient’s day to day functioning (Russell, et al., 2007). Most patients diagnosed with Alzheimer disease are over 65 years old although the Alzheimer process can start earlier. In 2010, there were 27 million people diagnosed with Alzheimer’s disease. It is projected that by the year 2050, 1 in 85 people globally will be suffering from Alzheimer’s disease (Holscher, 2011). Research has associated the disease with plaques and tangles in the brain. Alzheimer’s disease is characterized by loss of synapses and neurons in the cerebral cortex and some areas of the sub cortical regions. This leads to loss in gross atrophy of the affected parts of the brain (Irwin, 2010). In Alzheimer’s disease, an unknown protein causes amyloid precursor protein to be divided into smaller fragments by enzymes in a process called proteolysis. One of these fragments becomes fibrils of beta-amyloid that form deposits in dense formations referred to as senile plaques. A protein called tau stabilizes microtubules. In Alzheimer’s disease, tau undergoes chemical changes and begins to pair with other threads that creates neurofibrillary and disintegrates the neuron transport system (Thompson, et al., 2007). Type 2 Diabetes Mellitus Type 2 diabetes is the most common form of diabetes. Unlike type 1 diabetes, the bodies of type 2 diabetes patients make insulin, but either the body does not use the insulin well or the pancreas does not make enough insulin. This condition is referred to as insulin resistance. When the body does not have enough insulin or the insulin is not being used as it should be, glucose cannot enter the body cells (Ott, et al., 1999). The glucose starts to build in the blood instead of getting into the cells. This makes the body cells not to function properly. Type 2 diabetes is mostly common among the adults but recently studies show that type 2 diabetes is also increasingly affecting children as obesity among children increases (Irvine, 2010). Type 2 diabetes mainly affects people over the age of 40 years. However, the disease is also affecting young people nowadays. In the United Kingdom, type 2 diabetes is starting to affect obese people no matter the age. The disease is caused by insufficient insulin production from the beta cells. Insulin resistance occurs primarily within the liver, muscles and fat tissue. Insulin resistance leads to inappropriate releases glucose into the blood. The glucose levels may differ between different individuals. There is also increased breakdown of lipids in the fat cells and lack of incretin. There is also increased retention of salt and water by the kidneys and the central nervous system causes irregular metabolism. However, it is important to note that not all people with insulin resistance develop diabetes because impaired production of insulin by the pancreatic cells is a factor (Holscher, 2010). Insulin Resistance A disturbance in insulin production in the body is a sign of cell growth impairment. Insulin not only regulates the levels of blood sugar in the blood, but it is also a factor in the growth of on all body cells including neurons in the CNS. Therefore, insulin resistance causes several degenerative processes. These degenerative processes contributed to Alzheimer’s disease while the insulin imbalance cause type 2 diabetes (Holscher, et al., 2008). Therefore, some pathological processes between Alzheimer’s disease and type 2 diabetes are similar. Dyslipidemia Studies have shown that inefficient sleep patterns are associated with increased risk of type 2 diabetes, dyslipidemia and hypertension. The study was on a group of elderly Alzheimer patients’ caregivers. The study suggested that sleep duration is not necessarily associated with type 2 diabetes, dyslipidemia or hypertension. Inflammation Type 2 diabetes alters some components of the immune system. The biggest changes occur to the adipose tissue, pancreatic islets, the liver, the vasculature and circulating leukocytes. The alterations include levels of cytokines and chemokines and increased apoptosis and tissue fibrosis. These changes suggest inflammation occurs in the pathogenesis of type 2 diabetes. Inflammation also occurs in the pathological vulnerable regions of the Alzheimer’s disease. The degenerating tissue and deposition of insoluble materials are significant catalysts for inflammation. Animal models and researches done suggest that Alzheimer’s disease inflammation plays a big role in Alzheimer’s disease pathogenesis (Fendt, et al., 2010). Similarities between physiological processes underlying T2DM and AD Type 2 diabetes and Alzheimer’s disease share common physiological features. The common impairment between these two diseases is insulin imbalance. The insulin imbalance affects cell differentiation, cell growth, cell repair mechanisms, glucose utilization and energy metabolism. Insulin resistance leads to disintegration of neuron cell (Holscher, 2006). Other signaling systems such as insulin growth factors and transforming growth factors are also affected in both conditions. Misfolding of cells also plays a critical role in both diseases as well as the aggregation of amyloid peptides and cytotoxic developments which lead to a programmed cell death. This increases the chances of both diseases progressing. Epidemiological studies that link T2DM and AD A study conducted in Rotterdam showed that patients suffering from Type 2 diabetes had higher chances of developing Alzheimer’s disease. Further epidemiological studies have been conducted that prove that fact to be true. The link between these two conditions has raised serious concerns in the medical fraternity. There are more than 20 million Type 2 diabetes patients in the United States. About 18 million of Type 2 diabetes have more than 50% chances of developing Alzheimer’s diseases compared to people who do not suffer from diabetes. However, as research continues there is a chance that Type 2 diabetic and Alzheimer patients may live longer (Holscher, 2005). Amyloid Peptides Studies show that patients suffering from alzheimer’s disese have high frequency of islet amyloid. However, the same cannot be said for patients with Type 2 diabetes. The duration for which a patient has been suffering from Type 2 diabetes is a major factor on the frequency of islet amyloid. There is close resemlbace in pathology in the brain of a person suffering from alzheimer’s disease and that of a person suffering from Type 2 diabetes. The similarity is attributed to amyloid deposits with gradual reduction in the number of cells of proteins. Amyloid deposits are cytotoxic and may lead to disruption of protein cell membranes in both diseases. NFTs and Hyperphosphorylated Tau Protein Tau protein abnormalities is said to initiate the Alzheimer’s disease process. A hyperphosphorated tau pairs with other tau threads. Eventually, they form neurofibrillary tangles (NFT) inside nerve cell bodies (Julien, et al., 2010). This leads to disintegration of micro tubes and the collapse of the neuron’s transport system. This affects the chemical communication between neurons causing the death of cells. Therefore, a person suffering from Type 2 diabetes has a higher risk of developing Alzheimer’s disease because of the insulin resistance and disintegration of cells. That implies that these diseases are connected and share pathological processes. Glyceraldehyde-derived advanced glycation end products (AGEs) and O-linked N-acetylglucamine acylation Oxidative stress plays a crucial role on the way diabetic complications develop. Anomalies in the metabolism process cause mitochondrial superoxide overproduction. The increase in superoxide production leads to activation of major pathways in pathogenesis complications. It increases expression of the receptor for AGEs and its activating ligands and activation of protein kinase (Hardy and Selkoe, 2002). Carbonyl compounds react with amino groups to form AGEs. Hyperglycemia is not the only factor in diabetic complications. An increase in intercellular fatty acyl-CoA in the beta cell also plays a major and can accelerate Alzheimer’s disease (Li, 2007). TGF-B A decrease in signaling through T-beta receptors can lead to dementia. Transforming growth factor beta is a protein that controls cell differentiation and proliferation of cells. TGF-B plays an important role in regulating glucose and energy homeostasis. A high concentration of TGF-B in the blood and the cerebral spinal fluid plays a major role in neurodegenerative cascade which leads to Alzheimer’s disease and pathology (Hamilton, et al., 2011). Insulin resistance can lead to an increase in the concentration of TGF-B in the blood. Therefore, that increases the chances of a person suffering from Type 2 diabetes developing Alzheimer’s disease. Therefore, TGF-B plays a major role in the pathology of both diseases (Hooper, 2012). Evidence from Animal Models Recent research using animal models has led to the identification that shows that there are shared mechanisms between Alzheimer’s disease and Type 2 diabetes. However, Alzheimer’s disease pathology is more severe than Type 2 diabetes animal models exhibiting insulin resistance (Li, et al., 2009). It has been suggested that hyperinsulemia and insulin resistance represent important factors in Alzheimer’s disease and Type 2 diabetes. The study also showed that cerebral vessels which make up important substrate are damaged by the two diseases (Wang, et al., 2010). The evidence collected from animal models has provided important information that that could help in identifying potential treatment targets in Alzheimer’s disease. Results from animal models also show that the pathological processes in the central nervous system and the body are very similar. Conclusion Alzheimer’s disease and Type 2 diabetes mellitus have been discussed, and contrasting arguments evaluated. Although these contradictory arguments have been explored, the overall outcome of this discussion is that the statement “Apart from the anatomical location, pathological processes in the CNS and the rest of the body are very similar” is correct. However on the whole the pathological processes of these autoimmune diseases are more complex than this statement allows. Alzheimer’s and type 2 diabetes mellitus demonstrate that pathological processes are similar. The only thing that is different is the anatomical location the process is taking place (Li, et al., 2007). However, both can still be described to fit the statement because the pathological processes involved in Type 2 diabetes can lead to Alzheimer’s disease. There is growing evidence that link amyloid deposition in the brain and pancreas with pathogenesis of Alzheimer’s disease and Type 2 diabetes. Given the similarities, it follows that there is a common underlying mechanism between islet and cerebral amyloid. Diabetes type 1 mellitus provides the weakest evidence since there is no similarity its pathological process and Alzheimer’s pathological process. The final conclusion is therefore that, on the whole, this statement can be used to describe the pathological process of these degenerative diseases. References Abbas, T., et al., 2009. Impairment of synaptic plasticity and memory formation in GLP-1 receptor KO mice: Interaction between type 2 diabetes and Alzheimer's disease. Behavioral brain research, 205 (1). pp. 265-71. Fendt, M. et al., 2010. The effect of mGlu(8) deficiency in animal models of psychiatric diseases. Genes, brain, and behavior, 9. pp. 33-44. Hamilton, K., et al., 2011. Novel GLP-1 mimetics developed to treat type 2 diabetes promote progenitor cell proliferation in the brain. J Neurosci Res, 89. pp. 481-489. Hardy, J., and Selkoe, D., 2002. 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