Alzheimer’s Disease Bruce Seumanutafa
March 3, 2013
Western Oregon University
HE 434W Diseases
Professor Neilann Horner
Alzheimer’s disease is a very common disease that stems from dementia with no cure yet discovered. As there is no known cause for the disease, scientists do believe it is chemically related to changes in the human brain. In this paper many elements of this disease will be discussed and defined. The disease definition, diagnostics of this disease, the epidemiology of Alzheimer’s, many things related to treatment, as well as resources available to those affected by Alzheimer’s disease is all included.
Senile dementia which is also known as Alzheimer’s disease (AD) is the most common form of dementia. When the brain loses function and capability to form and retain memory it is called dementia. Alzheimer’s disease is an irreversible, progressive brain disease that results in loss of memory as well as cognitive function. Slowly symptoms develop and progressively get worse as time goes by, becoming so severe daily tasks are close to impossible. In many cases Alzheimer’s can ultimately lead to death because there is no cure. (NIA, 2008)
Although the direct cause of Alzheimer’s is unknown, there are characteristics that could increase the chance of getting this disease. People are more likely to get Alzheimer’s with age, but it is important to know that developing Alzheimer’s is not a normal part of aging. Getting Alzheimer’s has been related to genetics meaning if a close blood relative such as a brother, sister or parents have the disease your odds are higher. Also, people with higher risk have genes linked to Alzheimer’s such as APOE epsilon4 allele. (NIA, 2008)
Alzheimer’s disease compromises the brains neurons to effectively communicate with one another. By two abnormal structures that are called beta amyloid plaques and neurofibrillary tangles. “Specific proteins in the neuron’s cell membrane are processed differently and forms beta amyloid plaques.” (NIA, 2008) The enzyme Alpha-secretase snips the amyloid precursor protein and releases a fragment. Gamma-secretase, the second enzyme comes along and also snips the amyloid precursor protein. These snipped fragments normally benefit neurons, but with Alzheimer’s disease it actually harms them. With AD the first snip is from the enzyme called Beta-secretase. With the cut from the Beta-secratese combined with the snip from the Gamma-secretase it causes the release of short fragments of Beta-Amyloid. After being released, these fragments clump together becoming toxic and corrupt the functions of the neurons. As more and more fragments are added, the clumps increase in size eventually forming Beta-Amyloid plaques. (NIA, 2008)
The second abnormal structure is the neurofibrillary tangle and is made when a protein called tau is modified. Normally in brain cells, the tau protein acts as a stabilizer to structures that are crucial to the cells internal transport system. Microtubules are structures where nutrients and other cellular cargo are carried up and down to all parts of neurons. With Alzheimer’s disease, abnormal tau protein separates from the microtubule structure and causes them to fall apart. Strands from the protein combine and form tangles inside of the neuron which results in the disabling of the transport system (NIA, 2008). This ultimately destroys the cell as neurons in certain brain regions tear apart from each other and die. This causes memory loss.
Alzheimer’s disease exhibits signs and symptoms just like any other disease. Early symptoms of Alzheimer’s include the difficulty of performing daily tasks that once were easily accomplished as well as having trouble learning new information or routines. Getting lost on familiar routes and having trouble finding or remembering the names of familiar objects