Case Study Of Alzheimer's Terminal Neural Degenerative Disease

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

1.1 Dementia is an umbrella term for a range of diseases that affect memory, behaviour and motor skills. The causes vary depending on the disease but largely the presence of “plaques” and “tangles” on the neurons of the brain is found in people with Alzheimer’s. Plaques are protein that the body no longer breaks down and allows to build up; these get between the neurons and disrupt the message transmission. Tangles destroy a vital cell transport system made of proteins. The transport system is organised in orderly parallel strands like rail tracks. In healthy areas a protein call “tau” helps the tracks stay straight but in areas where tangles

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

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 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.

Even though people are free of symptoms during the pre-clinical stages, toxic changes are taking place in the brain. MRI scans show that the brains of people who are in the first stages of Alzheimer’s disease are forming thick clumps of hard proteins called beta-amyloid plaques and tau tangles. The damage quickly spreads to a part of the brain called the hippocampus, which is responsible for forming and storing memories. As the disease progresses, the brain begins to shrink and wither as nerve cells die and nerve connections are lost. By the final stages of Alzheimer’s disease the damage is widespread and brain tissue has atrophied and shrunk significantly and victims are unable to perform even the simplest of tasks. (Alzheimer’s Disease;

“Alzheimer’s disease is a progressive condition that destroys the connections between cells in the brain.” (WebMD, 2014). As the cells die the cortex shrinks. The part of the brain that is impacted the most in dementia is the cortex. The cortex includes the hippocampus. This helps new memories form. If there is damage to this part of the brain, there will be problems with the person memory.

Under normal condition tau binds to microtubules, stabilizing neuronal structure and integrity. Hyperphosphorylation of tau is assumed to be the cause of the formation of paired helical filaments - neurofibrillary tangles (NFT). The principle components of the senile plaques are neurofibrillary tangles in the cell bodies, neuropil threads, and neurites as well as extracellular A-beta amyloid. These lesions are surrounded by microglial and astrocytes. The brain regions affected by Alzheimer’s disease also contain neuritic or senile plaques in which extracellular deposits of amyloid are surrounded by dystrophic axons as well as the process of astrocytes and microglia. The principle constituent of amyloid is a 4kDa peptide called A-beta amyloid. A-beta amyloid is cleaved from a larger precursor protein called amyloid precursor protein. Similar abnormalities occur in transgenic mice with mutant APP and in individuals with Alzheimer’s

Alzheimer’s disease is a degenerative disease of the brain that causes gradual loss of memory, judgement and ability to function. This age-related, non-reversible brain disorder develops over a period of years. This disease is named after Dr. Alois Alzheimer. He had noticed changes in the brain tissue of a women who had died of an unknown mental illness. Alzheimer’s usually appears in people over the age of 65 but earlier stages of Alzheimer’s is created throughout adulthood. The early stages of Alzheimer’s is yet unknown but the damages to the brain is said to be caused up to a decade earlier before the problems become evident. Amyloid plaques, neurofibrillary tangles, and neurons, being the loss of connection between nerve cells, are the main features in Alzheimer’s disease. Abnormal deposits of protein form amyloid plaques and tangles throughout the brain and the at once healthy brain begins to work less efficiently. Over this time, neurons then lose the ability to function and communicate with each other and they eventually end up dying. The damage caused by this soon spreads to a near structure in the brain called Hippocampus. Hippocampus plays important roles in the the brain such as long-term memory. As more and more neurons tend to die, the affected parts of the brain begin to shrink. By the final stage of Alzheimer’s, the damage has spread throughout the affected patient’s brain and the patient’s brain tissue has significantly shrunk. Alzheimer’s disease can also be

Alzheimer’s disease is an irreversible, neurodegenerative disease that affects the brain causing progressive memory loss and destroys thinking skills. Alzheimer’s is the most common type of dementia, which is a general term used to describe disorders that affects brain functions. Alzheimer’s disease is caused by formations of plaques and tangles in the brain. A dangerous protein called beta-amyloid tends to build up over time in the brain. As this protein molecule accumulates, they start to form plaques, which can damage and destroy brain cells. While plaques affect the spaces between the brain cells, an abnormal protein known as “tau” starts affecting inside the brain cell itself. “Tau tangles can interfere with the transportation of nutrients in and out of the cells, causing brain cells to degenerate and die” (Kosik & Bowman, 2015, p. 5). Some common symptoms for Alzheimer’s include memory loss, constantly misplacing things, unable to remember the names of family members, unable to communicate properly, and losing the ability to complete simple daily tasks. Alzheimer’s disease is a fatal disease, but patients don’t die from the disease itself. Advanced Alzheimer’s increases vulnerability and increases the chance of developing infections that soon lead to death.

There is a great deal of impetus for understanding the mechanisms that lead to clinical AD and discovering modifiable risk factors. Clinical symptoms of dementia relate to the affected areas of the brain. In AD the symptoms are caused by a progressive loss of cholinergic function due to neuronal cell death in the hippocampus and cerebral cortex, brain regions involved in thought processing and memory. At the microscopic level, the neuropathological hallmarks of AD consists of two kinds of protein aggregates, amyloid plaques and hyper-phosphorylated tangles of tau-protein (Figure 1). Amyloid precursor protein (APP) is a transmembrane protein without known function that is constitutively cleaved

The causes of Alzheimer’s are not yet fully understood; however, its effect on the brain can be understood. Alzheimer’s disease - insidious, attacking and terrifying - stalks and then murders brain cells. A brain afflicted with Alzheimer’s disease has a decreased count in cells and connections among cells. The more brain cells die, the smaller the brain of a person with Alzheimer’s gets. When doctors examine a brain with Alzheimer’s tissue, they see two types of deformities that are known to be trademarks of the disease. The first trademark is known as plaque, which is a cluster of a beta-amyloid protein that may damage and kill brain cells in a number of ways, including blocking with cell-to-cell communication. Whereas the final cause of brain-cell death in Alzheimer’s remains a mystery, the groups of beta-amyloids that cover the brain cells are a sure sign of the disease. The second trademark of Alzheimer’s is the tangle. Brain cells are reliant on internal support and a transport system to bring nutrients and other essentials to their distant regions. This system needs a protein called tau. In Alzheimer’s, strings of tau protein roll into abnormal tangles inside brain cells, concluding in failure of the cell's transport system. This breakdown of the system is powerfully involved in the decline and death of brain

Cognitive impairment associated with Alzheimer’s disease occurs when synapses, which transmit information from one neuron to another, become interrupted and communication ceases (7). The result is death of the nerve cell within the brain, also referred to as synaptic failure (6). Synaptic failure takes place when amyloid plaque and neurofibrillary tangles develop (7). Amyloid plaque develops from amyloid beta proteins, which are released by enzymes from the amyloid precursor protein that is located on the surface of the neuron (7). The amyloid beta proteins are normally cleared within the body once they are released however, in

Alzheimer’s is a type of dementia that causes complications with memory, thinking, and behavior. Long before any signs of memory loss, there a microscopic changes occurring in the brain, altering its functionality (Alzheimer 's Association Organization, 2016). The brain has billions of nerve cells that work together, and when one portion of the brains neurons are malfunctioning it leads to breakdowns in other parts of the brain. The two most noted abnormal structures that are suspected to damage and kill neurons in the brain in patients with Alzheimer’s are plaques and tangles. Plaques are deposits of a proteins fragment called beta-amyloid that build up in the spaces between nerve cells; and tangles are twisted fibers of another protein called tau that build up inside cells (Alzheimer 's Association Organization, 2016).

Alzheimer’s disease is a progressive mental deterioration that can happen in middle or old age, due to generalized degeneration of the brain. Alzheimer’s disease is one form of dementia that gets harmful over time. Dementia is a loss of brain function that occurs with other diseases such as Alzheimer’s. Scientists believe that Alzheimer’s disease results from genetics, lifestyle, and environmental factors that impact the brain. Alzheimer’s disease damages and kills brain cells and it also leads to brain shrinkage. In the brain tissue there are two types of abnormalities that are considered toward the disease, Plaques and Tangles. Plaques are clumps of proteins that may hurt and destroy brain cells. Tangles are a system that requires the normal structure and functioning of a protein. There are many symptoms when it comes to Alzheimer’s disease. For example, memory, you forget conversations you had, misplace possessions, and eventually will forget the names of everyday objects and family members. Overtime you forget how to speak, write, and think. There are also changes in the personality such as depression, anxiety, mood swings, changes in sleeping habits, and even wandering. There are two drugs that are used to slow down the process of Alzheimer’s since they have not found a cure. The first drug is called Cholinesterase Inhibitors, which is a drug for boosting levels of a cell-to-cell communication. The second drug is called Memantine, which works with another brain