Ad : An Unidentified Mystery

Alzheimer 's disease (AD) is a progressive degenerative disease of the brain from which there is no recovery. There are three brain abnormalities that are the hallmarks of the Alzheimer’s disease is initially caused by plaques buildup in the brain’s neurons as illustrated in figure 1. The support structure that allows the flow of the nutrients through the neurons gets damaged and ultimately there is loss of connection among the neurons and they die off (National Institute of Health, 2015). This causes the brain tissue to shrinks, which is called atrophies. All this ultimately lead the victim of this disease to face difficulties in governing emotions, recognize errors and patterns, coordinate movement, and remember. Ultimately, a person with AD loses all memory and mental functioning.

Alzheimer’s disease (AD) is a progressive and fatal form of dementia, frequently seen in the elderly altering their cognition, thought process and behavior. AD is reported in about half of patients that have a dementia diagnosis; one study states that about 10.3% of the population over 65 years is affected by dementia with an increase to almost 50% over the age of 8 (Beattie, 2002). Alzheimer’s disease is not a normal part of the aging process in humans, but rather found in a group of diseases that affect the brain leading to a decline in mental and physical control. AD when diagnosed has a very slow and gradual course, initially affecting the individual’s short term memory (Beattie, 2002). Alzheimer’s disease is the 6th leading cause of death, affecting more than five million people in the United States and is also one of the most common forms of dementia. Dementia can be defined as a disorder of progressive cognitive impairment severe enough to affect daily functions of an individual’s life (Fillit, et al., 2002).

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

The brain changes in size and weight as a person ages. There is also a narrowing of the gyri, enlargement of the ventricles, and widening of the cerebral sulci. In AD, these changes are accelerated, causing issues such as atrophy of the cerebral cortex and loss of cortical neurons. In addition, the pre-central gyrus of the frontal lobe, superior temporal gyrus, hippocampus, and substantia nigra are all affected. Changes in neurofibrillary tangles (tangled masses of fibrous tissue throughout the neurons) , amyloid-rich senile or neuritic plague (degenerating nerve terminals in the hippocampus which contain proteins that form neurotoxic plague in the brain) and granulovascular degeneration can all occur as well.

One hallmark of AD is amyloid beta plaques, large aggregates found in the patient brains composed of the peptide, amyloid beta. These amyloid

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.

The research into Alzheimer's Disease has come a long way since 1906 when it is was discovered by Alois Alzheimer. He detected microscopic brain tissue changes called senile and neuritic plaques in deceased patients. These are chemical deposits consisting of protein molecules called Amyloid Precursor Protein(APP) that are fundamental components of a normal brain. However in the brain of an Alzheimer patient, an enzyme cuts the APP apart and leaves fragments in the brain tissue. These combined with degenerating nerve cells cause the plaques or lesions. These lesions are found in many sections of the brain including the hippocampus which regulates emotion and memory, the basal forebrain, and especially the basal nucleus of Meynert and the cortex, where the memory function is located.(2) Another sign of a diseased brain are neurofibrillary tangles, which are malformations within nerve cells.

This specific gene codes for amyloid beta peptides. The amyloid beta peptides are found in the plaques associated with AD and also in the neurofibrillary tangles. Accumulation of this peptide may cause AD. There is usually too much accumulation of amyloid beta in the brain and not enough clearance. The build up then causes the plaques and tangles. It is believed that a missense mutation in the precursor for this peptide is what causes an imbalance between accumulation and clearance. Also, when the amyloid beta forms deposits in the neurons, it is believed to stimulate activity of microglial cells. When these cells are stimulated, it causes the production of more amyloid beta, accounting for the progression of the disease. This theory is known as the amyloid beta cascade hypothesis. Although there are many supporters of this theory, there still is not enough evidence to prove it and there is some evidence against it. Firstly, there is not a mutation in the amyloid gene that increases the risk of familial AD. Amyloid beta has also been shown to be non toxic, so it alone can not account for the death of neurons in the brain associated with AD. However, the stimulation of the microglial cells also results in the production of tau proteins, which when in excess, may be the cause of neuronal death. Also, the microglial activation might cause the release of other neurotoxic molecules, such as IL-1b, IL-6, TNFa, nitric oxide, and many other

A standout amongst the most energizing methodologies of treatment is utilizing β-amyloid antibodies to assault the malady. Discovering approaches to let down levels of β-amyloid is a key step towards the curing AD, and hereditary qualities assumes a significant part in this procedure. A change in the quality Apoe that advances the arrangement the β-amyloid into neuritic plaques is the initially ensnared in the hereditary qualities of the illness. Understanding the first occasion that happens, and what happens to a well-working cell to prompt the onset of the sickness is essential (The Alzheimer's Project, 2009). The larger part of individuals diagnosed with AD have the late-onset variations. Then again, concentrating on the early-onset cases has been the best hotspot for exploration in discovering a cure for the

Alzheimer’s disease, also known as Alzheimer's or AD, is a neural disease that slowly gets worse over time. Alzheimer’s is the most common cause for dementia. There is currently no cure for Alzheimer's. The chances of getting this disease increases substantially after age 70 although you can get it earlier, though the chances will be smaller. The main risk factors for Alzheimer's is increased age, although genetics may play a role in getting this disease.Some symptoms or stages of Alzheimer's is; loss of orientation of place or time, poor planning or judgement, and losing or misplacing items. Alzheimer's is a slowly progressive disease of the brain that is characterized as memory loss. Although the risk for getting Alzheimer's increases as you age, it is not however a normal part in aging.

In Alzheimer’s two things have been shown to cause this disease in people; tangles and tau plaques. Plaques are sticky deposits of protein called beta amyloid; however, normal cells make this protein. It is formed from another protein called amyloid precursor protein, or as it is commonly known as APP. Cells use enzymes on their surface to make beta amyloid out of APP. The enzymes act like scissors, cutting beta amyloid from the bigger APP molecules. Usually, beta amyloid proteins dissolve after it drifts away from the nerve cell, but when the abnormal enzyme “ships” the APP to a different location, they begin to form into insoluble clumps: fibrils. Fibrils cluster together creating the plaques seen in AD

The pathophysiology, how the disease affects the body, is important when trying to understand Alzheimer’s. Damage to the brain in someone with Alzheimer’s starts around a decade before memory problems appear (NIH). Damage to the brain is symptom free during this period, but toxic changes are occurring in the brain. Alzheimer’s is mainly characterized by plaques and tangles in the brain that form from abnormal deposits of proteins (NIH). Plaques form when beta-amyloid, protein pieces, clump together (alz.org). Beta amyloid is chemically sticky and slowly accumulates between nerve cells and eventually forms plaques (NIH). These plaques block cell to cell signaling at the synapses (alz.org). In a normal and healthy brain, the brain is organized

Advancing age is the biggest risk for AD, with every decade after 65 years of age doubling the risk for AD. Family history is the second strongest risk factor following age. Studies conducted over the last three decades have shown that the genetic factors leading to AD are complex and heterogeneous, meaning, AD risk is attributed to a complex interaction of heritable (e.g. genetic) and non-heritable (e.g. education, life-style) factors. Although environmental factors do affect AD risk, population and twin studies estimate up to 80% of the AD cases are attributable to genetic risk factors (Gatz et al., 2006).

Another clue may be the effects the aging process has on the brain as it is harming the neurons in the brain causing the disease (NIA, 2012). Regardless of the cause, AD is a life altering disease in every aspect of the victim’s life.

Alzheimer 's disease (AD) the commonest form of dementia (70 %). It is a complex disease which is characterized by an accumulation of β-amyloid (Aβ) plaques and neurofibrillary tangles composed of tau amyloid fibrils associated with synapse loss and