Alzheimer 's Disease And Its Effects

Alzheimer 's disease (AD) was discovered by a German doctor Alois Alzheimer in 1906 when he found amyloid plaques and neurofibrillary tangles in the autopsy of a woman who died of an unknown mental disease. The extracellular amyloid plaque deposits, composed of insoluble amyloid-Beta peptide were hypothesized to be the main etiological factor. “The most important abnormality is an excess of Amyloid-beta peptides brought about through either overproduction or failure in degradation.” (Uzun, Kozumplik, & Folnegović-Smalc, 2011) Later, it was discovered that intracellular neurofibrillary tangles composed of hyper-phosphorylated, helically-paired tau

Alzheimer’s disease is a neurological disorder, in which one progressively loses memory, thinking skills, and the ability to perform activities of daily living. Alzheimer’s is a form of dementia also called senile dementia, and two thirds of dementia cases are from Alzheimer’s disease (ZZZZ). This disease usually effects the older generation, early 60s to late 60’s. According to the National Institute of Aging, over 5 million Americans have Alzheimer’s, and it is ranked the sixth leading cause of death (ZZZZ). This disease is caused by changes in the brain. Researchers noted these changes were a buildup of abnormal plaques called, amyloid plaques, a lost connection between nerve cells and the brain, and also fibers in the brain become tangled. Also this is a genetic disease, and environmental factors also play a role in the onset of this disease. These characteristics are said to cause the onset of Alzheimer’s disease (ZZZ). Alzheimer’s disease has many onset symptoms. The most common symptoms of this disease are memory loss and confusion. Examples of this is asking the same question and not realizing it, and not remembering where things are. These symptoms progressively worsen to the person forgetting who their family members are, and eventually not being able to function on their own.

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.

The topic of this article is about the effects that Alzheimer’s has on the patients, family members/caregivers. I believe there is a grave importance in this topic to help understand the effects of this disease and possibly help farther research. This might bring a few questions to the front of this discussion. How the relationship is after a patient is diagnosed with Alzheimer’s? How does this effect the family members/caregivers? What symptoms do family members experience with Alzheimer’s patients? What factors in life play a role in developing this disease? This paper will explore these questions with the respect of these news articles.

Alzheimer’s disease is the progressive loss of memory and mental functions. The disease affects memory, thought control, language, and other cognitive functions. The disease typically appears with old age and is often found age 60. Alzheimer’s causes the brain to develop clumps and tangles fibers in the brain tissue along with the loss of neuron connections. Throughout the brain, proteins are abnormally distributed and they form tangled bundles of fibers and amyloid plaques. Some neurons fail to function properly and lose their connections, which are necessary for the transmission of messages to the body. The hippocampus is the key brain structure in the formation of memories and often experiences the first signs of damage.

As AD is a progressive disease with no currently known cure, all current treatments are aimed at slowing the progression of the disease; these treatments have been available since 1993 (Geldmacher et al., 2011). The desired

Alzheimer’s disease is the most common type of dementia in the United States, with its commonness expected to increase dramatically in the coming decades. Although awareness of Alzheimer's disease has increased greatly among professional and amateur audiences, exact means do not exist to calculate how many Americans the disease affects. However, it is estimated that there are over 5.1 million people aged 65 or older with probable Alzheimer's disease. Alzheimer’s is also the sixth leading cause of death in America. Throughout, I will be addressing the issues that surround this disease: it is not an inevitable consequence of aging, the care and treatment, and end-of-life decisions. While explaining these issues, the goal is to achieve a better

“Dementia is characterized by chronic, global, non-reversible deterioration in memory, executive function, and personality. Speech and motor functions may also be impaired” (Butler and Radhakrishnan, 2011). As defined by Butler and Radharkrishnan, dementia is a disease that affects a person for their whole life. In the next part of this paper, I’m going to talk about the dementia and the effects it has on a person live whether it is with the symptoms, overall experience with it, and what exactly it does to the body. Dementia isn’t a fun disease to have or deal with. According to the World of Health Organization, over 35 million people have dementia (Robitaille, Garcia, & McIntosh, 2015). I’m mainly going to talk about the specific type of dementia Alzheimer’s. “Alzheimer’s disease is defined as a type of dementia characterized by an onset and slow deterioration, and involves impairments in memory, speech, personality, and executive function”(Butler and Radharkrishnan, 2011). Memory loss isn’t just the only thing that happens with dementia. They also experience impairments in language, communication, focus, and reasoning (Ellis, 2013).

It is a disease that we haven’t cured yet but instead have only come up and still coming up with treatment strategies to alleviate its symptoms. AD was first described in 1906 by a German psychiatrist by the name of Alois Alzheimer whilst he was performing a histophathologic study of his patient’s brain, a patient who had been suffering from dementia. His patient’s brain’s autopsy brought to light the presence of two types of lesions, which are senile plaques and neurofibrillary tangles. He saw a visible difference in the brain tissue for it was severely damaged by these lesions. Since then, our knowledge of AD’s cellular and molecular alterations has increased and we have come up with various hypotheses for AD that may soon help in developing effective preventative and therapeutic strategies. One of the most prevailing hypotheses that have already leaded to a number of therapeutic approaches is the amyloid cascade hypothesis. Hence, the following essay will explore the pathology of the amyloid cascade hypothesis and the evidence for and against it. It will also touch upon current progress in clinical trials that test the

Alzheimer's disease (AD) is a neurodegenerative disorder with relentlessly progressive losses in cognition, memory, and language. According to research by Herbert, Weuve, Sherr, and Evans (2013), 5.3 million people are affected by AD, and that number is expected to almost triple by the middle of the century. As cognitive decline progresses, independence and the ability to perform self-care is lost as caregivers must assume this considerable burden. Given the prevalence of AD, its devastating pathology, and its impact on loved ones and caregivers, the social impact of this disease cannot be overstated.

When looking into the future and thinking about what your life will be 10, 20, even 30 years down the road I would guess the majority of us picture our lives as carefree and exciting, in perfect health and rich. Maybe you have 5 kids, the perfect job and a cookie-cutter husband. Or maybe you travel the world, have a rockin’ body and work for the CIA. Unfortunately that isn’t the outcome for everyone. There are those who will develop Alzheimer 's dementia.

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

In the next stages of AD, more genitive damage is evident as well as problems with expression, emotion, language, and reasoning. In the middle stages of AD patients have trouble identifying people they know, they are unable to learn new things, and they are very uninhibited. The final stages are significantly different form the beginning and middle stages. In the final stage a person’s body begins to

The amyloid cascade hypothesis is the most widely accepted of the AD pathogenesis hypotheses. Its principle is that the accumulation of Aβ plays a major role in AD pathogenesis, and the disease is analyzed as a series of abnormalities in the process and secretion of the amyloid precursor protein (APP), where an inequality between production and clearance of amyloid β is the triggering event and the most important factor responsible for other abnormalities observed in AD (Hardy et al, 2002; Cummings et al, 2007). Amyloid β is a peptide with high resistance to proteolytic degradation. It consists of 37–43 amino acids with different isoforms (Deane et al, 2009). Aβ is the result of sequential cleavage of the amyloid precursor protein (APP), generating

Histopathologically, AD and FTD are different. In fact, AD is characterized by extracellular amyloid plaques and intraneuronal neurofibrillary tangles [5], and FTLD is characterized by non-AD histological pathology, most commonly by the presence of either tau-positive inclusions or ubiquitin-positive, TAR DNA-binding protein (TDP)-43-positive inclusions [6].