Relationship Between Cancer And Alzheimer 's Disease

Alzheimer’s Disease is a disease of the future. With the growing aged population, this disease, which affects primarily the elderly, will become of increasing relevance to the medical profession. Also, the high frequency of Alzheimer’s, and the high cost in labor, money, and material of caring for its victims shall put considerable burden on the society as a whole. Here, however, these issues are not going to be debated. Instead the pathology of Alzheimer’s will be reviewed to the extent it is known today.

Alzheimer’s disease is a prominent brain disease that effects a massive amount of individuals in the United States. Alzheimer’s disease (AD) is the sixth leading cause of death in the United States, accounting for 60-80% of dementia cases, with no chance of being cured, prevented or decelerating over time (Alzheimer’s Association, 2014). AD is the most well-known form of dementia, causing complications in brain function in the areas of memory, thinking, and behavior (Alzheimer’s Association, 2014). In an effort to gain a deeper understanding of Alzheimer’s disease, researchers create new knowledge about the disease, which is then distributed to the public. The goal in this information disbursement is to find new and inventive ways to treat AD, prevent AD from progressing at such a rapid pace, and aid in the quality of life in those diagnosed with AD as well as caregivers and medical professionals providing treatment to individuals’ with AD.

Due to the inability of the brain to replace nerve cells, some brain function is lost. The key question in Alzheimer’s disease is, what causes the neuron degeneration (Johnson, 1989)? The focus for finding the cause is on abnormal structures found in the brain of people with Alzheimer’s. Unfortunately, the abnormal structures the brain undergoes still has researchers uncertain as to how they are involved in Alzheimer’s and exactly how the disease occurs.

More than five million are living with Alzheimer’s disease in the United States and the number is set to almost triple by the year 2050. It is common in the elderly and generally occurs in persons over 65 years of age, but early onset of Alzheimer’s has also been documented (“Alzheimer’s disease facts,” 2016, para. 1). It starts in the medial temporal area of the brain, usually in the hippocampus, and then spreads to other areas of the brain. Blows (2011) explains, “Alois Alzheimer was a German psychiatrist who in 1906 described a dementia with two specific changes found in the brain after death... these changes were the presence of extracellular plaques and intracellular neurofibrillary tangles and these became the hallmarks of this disease” (p. 286). Loss of neurons takes place and amyloid plaques form. This is due to build-up of non-functioning proteins and can be observed by imaging techniques (Radin, 2003, p. 41). There are many risk factors that increase the risk of Alzheimer’s disease. The greatest risk factor is family history, but other risk factors include diabetes, hypertension obesity, hyperlipidemia, smoking, depression, physical inactivity, low estrogen levels, and head trauma (Huether & McCance, 2014, p. 546). The actual cause of Alzheimer’s is unknown, but there are genes associated with it that make the disease heritable. What is clear is that

Many scientists hypothesize that protein dysfunction plays a role in the progressive damage and death of nerve cells. The nerve cells may be blocked from communication

Alzheimer 's disease which chronically leads to Senile Dementia, is a horrific change in homeostasis for human beings. The most obvious change in homeostasis from Alzheimer 's is loss of memory. Memory loss can vary from short term to long term. Alzheimer 's disease has been occurring in humans for a long time. This is a disease that affects different body systems, and interrupts homeostasis to a significant point. As Alzheimer 's disease is further investigated, there are more discoveries with how it is caused, what it affects, and how to reduce the risk of developing it. Alzheimer 's disease is a frightening disease that is represented in humans. There are many concerns with this disease that are worth finding out for the future victims

Alzheimer’s, a severe irreversible form of dementia, is now a very prevalent issue in the aging population. Scientists are just beginning to understand what Alzheimer’s is, what causes Alzheimer’s and how to prevent it. Although research has come a long way, “Alzheimer’s disease, as science tries to grasp it, seems to slip through our fingers. The complex interaction of neurochemistry, genetics, environment, lifestyle and personality all play a part in how individuals experience Alzheimer’s. ~ Harry Clayton

As a medical practitioner, I was always fascinated by the complexities of the human nervous system. A few years later, during my neurology residency training, I developed special interests in the field of neurodegenerative disorders and dementias. These are largely non-curable disorders

Alzheimer’s disease is a form of dementia that can be directly related to a person’s age. The main physical manifestation of Alzheimer’s disease detects nerve cell deterioration which is demonstrated as an amplified loss of lucidity and a

Alzheimer’s Disease is 56% of the cause of dementia, which is characterized as a decline in memory language, problem solving, and other cognitive skills that affect a person’s ability to perform everyday tasks. (Petersen 2002) AD was first identified over 100 years ago, but it actually took about 70 years for it to be recognized as the most common form of dementia. (Alzheimer’s Association 2016) Although much has been researched and discovered about AD to help diagnose and treat the disease, much is yet to be discovered about the precise biological changes the causes Alzheimer’s and why it progresses more quickly in some than others. Scientists and doctors around the world have a common goal of discovering ways to stop of prevent this genetically

In 1906, Alois Alzheimer discovered Alzheimer’s disease after he studied the dead body of patient August D. An autopsy was done and found fiber tangles in the brain that is now known as amyloid plaques. During the autopsy, there was shrinkage in and around the nerve cells noted in the patient’s brain. The symptoms that August D experienced before she passed away were memory loss, paranoia, and psychological changes. Currently, the main features of Alzheimer’s disease still includes presence of plaques, tangles and the loss of connections between nerve cells in the

Alzheimer’s is a slow disease, taking 8 to 20 years from diagnosis to death. The main culprit of the infamous memory- loss disease is the beta amyloid protein. This protein builds up forming plaques. Beta amyloid also attaches to neurons first blocking synapses and eventually forming tangles by killing them. Over time more and more of these plaques and tangles accumulate while killing over 100 billion nerve cells. The damage these buildups of protein cause are tragic. Physically the brain shrinks; starting with the hippocampus and slowly progressing. However the changes the person affected with the disease encounters are far worse.

In addition, we wanted to assess whether astrocytes, the main ECM producers in the brain, become reactive already during this early stage of AD-like disease, thereby possibly contributing to the observed ECM alterations. Our preliminary results suggest no change in the expression of basigin, a downregulation of versican and tenascin-R, and an upregulation of HAPLN1 and glial fibrillary acidic protein (GFAP) in the hippocampus of APP/PS1 mice at 3 months (early AD). Although these changes are not completely in line with previously reported ECM alterations, we do find changes in hippocampal ECM in 3 months old APP/PS1 mice that may contribute to alterations in cell communication, neuronal survival, and synaptic function and plasticity. In addition, the observed increase in GFAP expression in the hippocampus of 3 months old APP/PS1 mice and in isolated hippocampal astrocytes in vitro suggests that astrogliosis precedes amyloid plaque deposition, thus astrocytes possibly play a role in early ECM

Specifically, nitric oxide has been identified contributing to neuroaxonal degeneration.1, 9, 10 Studies in the spinal cord and lateral geniculate nucleus in MS patients have shown a greater loss of small axons in comparison to larger ones.10 This is because smaller axons are more susceptible to inflammatory mediators like nitric

Subarachnoid hemorrhage (SAH), predominantly caused by a ruptured aneurysm, is a devastating neurological disease that has a morbidity and mortality rate higher than 50% [1]. Early brain injury (EBI) was reported as the primary cause of mortality and poor outcomes in SAH patients [2-4]. Therefore, novel therapeutic strategies aiming at elucidating EBI after SAH are required. It has been proven that a series of complex pathophysiological processes are involved in the pathogenesis of EBI. Among them, neuronal apoptosis plays a vital role [3,5,6]. Therefore, preventing neuronal apoptosis can be a prospective target to improve severe neurological deficits and outcomes in patients with SAH.