The Incidence Of Alzheimer 's Disease Essay

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 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.

Although Alzheimer’s Disease (AD) is the most widely known cause of dementia in the elderly population, there are many other explanations and clinical diagnoses that

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

Dementia is a syndrome which is progressive in nature, characterized by impairment of memory and loss of intellectual ability.1 Decreased level of Acetylcholine in the brain, neuro-inflammatory reaction, rise in the oxidative stress and hypercholesterolemia have been reported to play an important etiological role in the memory decline.2 Alzheimer’s Disease (AD) is the most common form of dementia which is a progressive and a neurodegenerative disease characterized by the presence of senile plaques rich in insoluble aggregates of β amyloid and neurofibrillary tangles in the brain. AD has been estimated to account for 50–60% of dementia cases in persons over 65 years of age worldwide.3 Alzheimer’s Disease International

Alzheimer’s disease (AD), is a type of dementia that no one would ever want their grandmother or grandfather to suffer from, as it destroys memory and other important mental functions of its sufferer. Alzheimer's disease is currently ranked as the sixth leading cause of death in the United States. While the age 65 and older is its target age, it has consumed the lives of over 1.9 million people. The brain begins to show signs of damage in the hippocampus, the part of the brain essential in forming memories. As more neurons die, parts of the brain then begin to shrink. By the final stage of Alzheimer’s, damage is widespread, and brain tissue has shrunk significantly. The idea that Alzheimer’s disease is related to age in 1974 was introduced

Alzheimer’s disease is an affliction that many families and individuals all over the world have to endure. As the individual slowly loses their memory and their ability to recognize themselves and others, they succumb to the disease soon after. Elderly people are most often associated with this disease, but a significant population under the age of 40 has shown symptoms of this disease. The positive news is that people, especially young people, can take precautionary measures to avoid being afflicted with Alzheimer’s. Researchers have conducted studies to determine whether Alzheimer’s is truly more prevalent in females rather than males. Alzheimer’s disease differs in how men and women are affected. It is essential to look at the physiological differences in men and women to fully comprehend the difference in prevalence factors. If medical professionals can better understand how the differences in AD in males vs. females, the better the treatments can be made available for certain genders. Treatments

“Alzheimer’s Disease (AD) is a type of dementia, which is affecting the population that develops in the brain and can lead to problems with memory, thinking and behavior”. The Amyloid Hypothesis claims that the build up of the beta-amyloid in the brain is a cause in the development of Alzheimer disease in patients. This plaque of the beta-amyloid and its cascade of events can be linked to the deterioration and negative effects of cognitive function of the brain over time. The beta-amyloid is described to be a “sticky” protein located in the brain therefore plaques or build up of the amyloid is common. These plaques in turn can block the brain cells from communicating with each other. Which then activates an immune system, that leads to inflammation

To understand how microbes may be involved in AD, we first must look at what physically happens to the brain with this disease. There are two distinct aspects involved in Alzheimer’s disease; beta-amyloid plaques and tau tangles. Beta-amyloid plaques are formed when the amyloid precursor protein (APP) which is present in the membrane of neurons (alz.org) is cleaved off by beta and gamma-secretases (Chen et al., 2001). In a normal brain, alpha-secretase does the cleaving and the body processes APP on its own (Chen, et al., 2001). In AD, the small pieces join to form beta-amyloid plaques but as smaller individual pieces they can interfere with nerve signaling

Alzheimer’s disease is among the sixth top leading causes of death in the United States and even with an estimated 4.5 to 5.4 million suffering from Alzheimer’s disease (AD) not much is known about the causes. Only the symptoms are addressed. The main characteristics of AD are degeneration of the ability to remember, reason, communicate and with loss of motor skills and function (Piazza-Gardner, 2013). Cognitive function that is lost and is accompanied by other physiological conditions such as depression, anxiety, irritability, aggression and inappropriate behavior for a setting or location that occur in most AD suffers (Senie, 2014). AD was noted as abnormal clumps and a bundle of proteins in the brain which was discover in patients with

Alzheimer’s disease (AD) is a progressive, terminal, degenerative brain disease. It is the fourth leading cause of death in adults and currently affects over four million people in the United States. This number is expected to increase over the next several years as the baby boomers age, until it reaches fourteen million by the year 2025.

Nevertheless, both types of AD are recognised pathologically by the build-up of intracellular neurofibrillary tangles, extracellular amyloid plaques, and massive neuronal and synaptic loss (Carmo & Cuello, 2013). Neurofibrillary tangles are aggregates of hyper-phosphorylated tau protein and plaques are mostly insoluble deposits of β-amyloid, resulting from the cutting of the amyloid precursor protein (APP) (Farooqui & Farooqui, 2011). The discovery of mutations in the APP gene which cause familial AD lead to the articulation of the amyloid cascade hypothesis (ACH) (Hardy & Asllop, 1991). A large amount of evidence supports this view; however a number of findings are contrary to its proposal. As a result, Armstrong (2011) proposed a revision of the hypothesis, postulating that the main trigger for the development of the disease is the ageing of the brain and related wear and tear such as head trauma and stress; collectively referred to as the “allostatic load” (Carroll, 2002). Furthermore, a greater emphasis has now been placed on the role of small, soluble amyloid oligomers which seem to be the cause of early cell dysfunction in AD, rather than the large, insoluble amyloid fibrils. (Ferreira, Vieira & De Felice, 2007).

The Aβ deposition and diffused plaque formation lead to local microglial activation, cytokine release, reactive astrocytosis and a multi-protein inflammatory response (Eikelenboom

Although Alzheimer’s disease (henceforth: AD) has been around since the 19th century or possibly even earlier and was at a point in time classified as senile dementia, it wasn’t until 1906 following Dr. Alois Alzheimer’s encounter with Auguste Deter at a Frankfurt asylum that the name of the disease was finally coined. Since then, major developments relating to the disease has taken place. In our report, we addressed some of the areas of the history, contemporary and prospects of the disease.

Our memories are priceless. It makes our life beautiful and worth living. Most importantly, it connects us with people around us. But what if those memories start fading away? What if it becomes difficult to remember names of people or places? This is the horror of Alzheimer’s, a form of dementia affecting millions of people across the globe. It is also one leading cause of death globally.