Description of Alzheimer's Disease
Alzheimer's Disease is a progressive neurodegenerative disorder that accelerates cell loss. The treatment costs of Alzheimer's Disease (AD) in the United States is estimated to be 100 billion. AD is the fourth common cause of death after heart disease, cancer and stroke. The neurobehavioral hallmark of probable AD is a gradual onset and continuous cognitive decline. The neuropathology of AD can only be confirmed by biopsy or autopsy which includes the presence of neurofibrillary tangles and amyloid or senile plaques. They occur in normal elderly persons but they occur in much larger numbers throughout the brains of AD patients and affect the functioning of the hippocampi. The brains of AD victims also have large numbers of granulovascuolar organelles which are small clusters of dead brain cell material that collect in the neurons in the hippocampi. Atrophy or shriveled cortex or shrunken cortex is a sign of dead nuerons that are present in Alzheimer's Disease.Scientists have so far identified one Alzheimer risk gene called apolipoprotein E-e4 (APOE-e4).
Today, the only definite way to diagnose AD is to find out whether there are plaques and tangles in brain tissue. To look at brain tissue, however, doctors usually must wait until they do an autopsy, which is an examination of the body done after a person dies. Therefore, doctors can only make a diagnosis of possible or probable AD while the person is still alive.
At specialized centers, doctors can diagnose AD correctly up to 90 percent of the time. Doctors use several tools to diagnose probable AD, including:
* questions about the person's general health, past medical problems, and ability to carry out daily activities, * tests of memory, problem solving, attention, counting, and language, * medical tests such as tests of blood, urine, or spinal fluid, and * brain scans.
Sometimes these test results help the doctor find other possible causes of the person's symptoms. For example, thyroid problems, drug reactions, depression, brain tumors, and blood vessel disease in the brain can cause AD-like symptoms. Some of these other conditions can be treated successfully.
No treatment can stop AD. However, for some people in the early and middle stages of the disease, the drugs tacrine (Cognex, which is still available but no longer actively marketed by the manufacturer), donepezil (Aricept), rivastigmine (Exelon), or galantamine (Razadyne, previously known as Reminyl) may help prevent some symptoms from becoming worse for a limited time. Another drug, memantine (Namenda), has been approved to treat moderate to severe AD, although it also is limited in its effects. Also, some medicines may help control behavioral symptoms of AD such as sleeplessness, agitation, wandering, anxiety, and depression. Treating these symptoms often makes patients more comfortable and makes their care easier for caregivers.
In recent years researchers have found that exercise improves memory,concentration, and abstract reasoning among older adults, and may even delay the onset of Alzheimer's disease. Aerobic exercise increases blood flow to the brain which nourishes brain cells and allows them to function more effectively. A recent study showed that exercise actually promotes the growth of new neurons(brain cells) in the hippocampus--the part of the brain that controls memory and learning. Scientists previously believed that once brain cells died, they were not replaced. According to previous research, chemicals, obesity, and smoking have all been linked to Alzheimer's. People who described themselves as goal-oriented and able to control impulses were less likely to develop Alzheimer's Disease according to a study of 997 people. Baby monkeys exposed to lead showed Alzheimer's like symptoms including amyloid plague, years later, according to a recent study. At the University of Alabama at Birmingham, mice who drank the equivalent of five sodas a day for six months did worse on memory tasks than those who drank water. The mice that had sodas had more than twice the amyloid plaque in their brains (which is a sign of Alzheimer's) than the others.
Someone develops Alzheimer's Disease every 71 seconds. As adults, the music we tend to be nostalgic for, the music that feels like it is "our" music, corresponds to the music we heard during the teen years. One of the first signs of Alzheimer's disease (a disease characterized by changes in nerve cells and neurotransmitter levels, as well as destruction of synapses) in older adults is memory loss. As the disease progresses, memory loss becomes more profound. Yet many of these old-timers can still remember how to sing the songs they heard when they were fourteen.
Two abnormal structures called plaques and tangles are prime suspects in damaging and killing nerve cells. Plaques and tangles were among the abnormalities that Dr. Alois Alzheimer saw in the brain of Auguste D., although he called them different names.
- Plaques build up between nerve cells. They contain deposits of a protein fragment called beta-amyloid (BAY-tuh AM-uh-loyd). Tangles are twisted fibers of another protein called tau (rhymes with "wow").
- Tangles form inside dying cells. Though most people develop some plaques and tangles as they age, those with Alzheimer's tend to develop far more. The plaques and tangles tend to form in a predictable pattern, beginning in areas important in learning and memory and then spreading to other regions.
Scientists are not absolutely sure what role plaques and tangles play in Alzheimer's disease. Most experts believe they somehow block communication among nerve cells and disrupt activities that cells need to survive.
History Behind Alzheimer's Disease
At a scientific meeting in November 1906, German physician Alois Alzheimer presented the case of "Frau Auguste D.," a 51-year-old woman brought to see him in 1901 by her family. Auguste had developed problems with memory, unfounded suspicions that her husband was unfaithful, and difficulty speaking and understanding what was said to her. Her symptoms rapidly grew worse, and within a few years she was bedridden. She died in Spring 1906, of overwhelming infections from bedsores and pneumonia.
Dr. Alzheimer had never before seen anyone like Auguste D., and he gained the family's permission to perform an autopsy. In Auguste's brain, he saw dramatic shrinkage, especially of the cortex, the outer layer involved in memory, thinking, judgment and speech. Under the microscope, he also saw widespread fatty deposits in small blood vessels, dead and dying brain cells, and abnormal deposits in and around cells.
The condition entered the medical literature in 1907, when Alzheimer published his observations about Auguste D. In 1910, Emil Kraepelin, a psychiatrist noted for his work in naming and classifying brain disorders, proposed that the disease be named after Alzheimer.