Alzheimer 's Disease And Its Effects

Autosomal dominant mutations in APP, PSEN1, or PSEN2 that alter APP processing and the production or self aggregation of Aβ, promote aggregation and accumulation of Aβ in brain causing early-onset AD (Bertram et al., 2010).

The loss of cognitive function is associated with fewer nerve cells and synapses than the normal brain. The neurons demise is thought to be from the formation of plaques and tangles. The formation of these plaques and tangles can begin many years before the person becomes symptomatic of AD. The formation of plagues comes from the breaking down of a protein in the cell membrane into protein fragments called beta-amyloid. The YouTube video, NIH: Unraveling the Mystery of Alzheimer's Disease, provides a clear animation how the beta-amyloid plaques are formed as these sticky fragments begin to clump together. (National Institutes of Health, 2011) The video shows another protein called tau, involved with formation of tangles. The tau protein is instrumental in the transport of food molecules, parts of cells, and key building materials and is compared to a railroad track system. The tracks become unraveled and form tangles. In the earliest stages of the disease, the plaques, and tangles form deep inside the brain in the medial areas where learning and memory are formed, then progresses toward areas where thinking and planning occur as the neurons begin to die. Because of the billions and billions of cells in the neuron forest, the damages caused by the plaques and tangles may go undetected and be asymptomatic for

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 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.

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.

the pathogenic mechanism of presenilin mutations which alters APP metabolism would be responsible to elevate levels of Aβ peptides. (Bertram and Tanzi, 2008). followed by APOE, a major genetic risk factor increase Aβ peptide aggregation and impair Aβ clearance in the brain for the disorder in the typical late-onset period (Strittmatter and Roses, 1995). The genetic studies suggest that neurodegenerative processes in AD are the consequences of an imbalance between Aβ peptide production and clearance. However, physiological functions of APP are poorly understood (Yoshikai et al., 1990; Ling et al., 2003; Muller and Zheng, 2012). The APP gene is located on chromosome 21 and those individuals suffer from Down's syndrome (trisomy 21) with an extra copy of this chromosome develops an early-onset familial AD (EOFAD) (Yoshikai et al., 1990; Ling et al., 2003). There are two proteolytic processing pathways of APP. In the non-amyloidogenic pathway, APP cleaved by α and γ secretases resulted in the production of soluble form of APP (sAPPα). In amyloidogenic pathway, APP cleaved by β-secretase generates membrane bound C-terminal fragment (C99) which subsequently cleaved by γ secretase and produces Aβ peptide (Nunan and Small, 2000; Selkoe and Schenk, 2003).

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

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.

According to data available from the Alzheimer’s foundation every 67 seconds someone develops Alzheimer’s disease and currently at least 5.3 million people are affected by the disease. The numbers are expected to grow as 75 million baby boomers transition into retirement by 2030. Alzheimer disease is a brain disorder that causes decay and dis- function of neurons resulting in memory loss, speech and language impairment. This can also extend to challenges in physical and social behavioural. The brain, consisting of the cerebrum, cerebellum and brain stem is the primary target of Alzheimer’s disease. At three pounds the brain has a network of arteries and a folded cortex that is responsible for memory and movement. These functions are facilitated by a network of neurons. Alzheimer’s disease interferes with these neurons by disrupting electrical transfer; Death of brain cells is inevitable as the cortex shrinks becoming incapable of developing thoughts and memory. The Alzheimer’s patient experiences an altered personality with family members becoming strangers.

Alzheimer disease (AD) is the most common cause of dementia in the elderly, accounting for 65–70% of all cases (Jellinger, Janetzky, Attems, & Kienzl, 2008). The other dementias are of the Parkinson 's group, the fronto-temporal group and the vascular group. The total worldwide yearly costs for the treatment and care of patients suffering from dementia are estimated to be around 250 billion US dollars. The lifetime risk for AD between the ages of 65 and 100 is 33% for men and 45% for women with an annual increase of 1–2% in the seventh decade to almost 60% in the 10th decade with doubling every 5 years (Jellinger et al., 2008). AD is incurable, and thus represents a major public health problem. AD represents a challenge to humanity due to its relatively recent discovery, progressive nature of the illness, and complex diagnosis.

“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).

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].

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