Alzheimer's disease (AD) is a degenerative disease of the brain from which there is no recovery. The disease slowly attacks nerve cells in all parts of the cortex of the brain and some surrounding structures, thereby impairing a person's abilities to govern emotions, recognize errors and patterns, coordinate movement, and remember. Ultimately, a person with AD loses all memory and mental functioning.
The major areas of the brain have one or more specific functions.
Alzheimer's disease is a disorder in which there is a steady deterioration of brain function, resulting in progressive loss of memory, recognition, personality, and mental powers. Although Alzheimer's disease may begin as early as age 40, it is most prevalent in the elderly. It accounts for about half of all serious mental impairment in persons over age 65.Changes in the BrainIn Alzheimer's disease, as in any senile mental disorder, there is atrophy (shrinkage or wasting) of the cerebral cortex (the outer layer of the brain, which is mostly concerned with intellectual and social functioning). There are also more specific abnormalities, such as the presence of tangles of fibers within the nerve cells and of senile plaques, which are probably deposits of amyloid (a semisolid protein complex seen in many degenerative diseases). These abnormalities are scattered through-out the cortex of a person with Alzheimer's disease; they distinguish the disease from other forms of senility. Because brain biopsy specimens (tissue samples taken from the brain for laboratory examination) are not obtained without very specific reasons and without intention of specific treatment, these abnormalities are usually discovered only after death.CausesTheories abound as to the possible causes of Alzheimer's disease. So-called slow viruses (viruses acquired early in life that take many years to do their damage) have been considered, as have environmental factors and damage from previous diseases. Recently, a diminished amount of the enzyme choline acetyltransferase (which is necessary to manufacture the neurotransmitter acetylcholine) has been found in some patients, and theories about replacement of the enzyme or the neurotransmitter are being formulated.Deficiencies of other neurotransmitters are constantly being discovered. Heredity seems to play some part, since a family history of the disease makes some individuals more likely than others to develop the condition. It is generally agreed that hardening of the arteries is not a cause. Alzheimer's disease does not appear to be contagious, nor is it caused by emotional upsets.SymptomsSymptoms vary considerably from one person to another and may occur days or months apart. They begin with small memory lapses, almost always first involving loss of recall for recent events. Such lapses can happen to anyone, but in Alzheimer's disease they grow more serious with time. A person may forget a close relative's name, get lost coming home from the office, forget to turn off the oven, misplace articles, recheck to see if a task was done, or repeatedly ask questions that have already been answered. Eventually, the gaps in memory and the failure to recognize friends and family members will interfere with normal life. As the disease progresses, the victim of Alzheimer's disease becomes confused, frustrated, and irritable. Although at first the person seems physically unaffected by the disease, as the condition advances, the patient becomes restless, always moving about, and must be watched so that he or she does not wander away or into danger. Endless repetition of unnecessary actions, such as the opening and closing of drawers, is another characteristic symptom of the disease. Some victims of Alzheimer's disease may even become extremely agitated with little or no provocation.The course of the disease may range from 1 year to as many as 20 years. The disease may eventually result in deterioration of the rest of the nervous system and other parts of the body and in loss of control over bladder and bowels. It may cut life expectancy by contributing to death from another cause, such as pneumonia or heart or kidney failure.
Can a study on reversing memory loss lead to new treatments for Alzheimer's?
Alzheimer's is a particularly tragic disease, devastating both those who suffer from it and their family members. Alzheimer's patients experience a loss of neurons (brain cells). This leads to a progressive loss of memory as well as loss of the ability to reason, communicate, learn and perform other tasks. Typically, Alzheimer's patients die four to six years after being diagnosed, though some live up to 20 years.
Five million people in the United States have Alzheimer's. Of those five million, 200,000 to 500,000 are under the age of 65, afflicted with dementias, including s early-onset Alzheimer's [Source: Alzheimer's Association]. There is no cure for Alzheimer's, but there are several different groups performing research to develop new treatments and possibly a cure. One new study, conducted on mice by researchers at MIT's Howard Hughes Medical Institute (with its findings published in the journal "Nature") offers exciting treatment possibilities.
Researchers have already discovered that a protein called p25 is linked to neurodegeneration found in Alzheimer's and similar diseases. The mice used in the MIT study are engineered so that the p25 gene can be turned on whenever the scientists desire. When the p25 gene is on, the mice develop a condition similar to Alzheimer's, characterized by a loss of neurons and brain atrophy.
Before activating the gene, the researchers, led by neuroscientist Dr. Li-Huei Tsai, taught the mice to associate a chamber with an electric shock -- called a "fear-conditioning test" -- and to navigate a maze. After the mice learned these tasks, the gene was turned on and the illness induced. It only took six weeks for the illness to erase the memories of the mice. They could no longer remember how to avoid being shocked or how to maneuver the maze with success.
Prior to this study, scientists already knew that a stimulating environment can promote learning in mice. However, they didn't know the effect of this type of environment on mice experiencing long-term memory loss (six weeks is "long-term" for a mouse). To test the effects of environmental cues on the mice, half the population was moved to a new habitat complete with engaging elements, including toys, exercise wheels and additional mice. The other group of mice was kept in an environment without any stimulation. After four weeks, the mice in the stimulating environment could remember the shock test and maze better than the mice in the non-stimulating environment. They could also learn new tasks better.
For Dr. Tsai and her team, the results were encouraging and pointed to a new possibility for the treatment of Alzheimer's disease. While the stimulation in mice didn't regenerate neurons, the treatment did promote the growth of new connections between existing ones. In other words, the neural networks of the stimulated mice re-established connections to previously "lost" memories. Dr. Tsai described the treatment as "actually rewiring the brain" [Source: Atlanta Journal Constitution].
A second part of the study conducted by Dr. Tsai's team involved treating mice experiencing neurodegeneration with a drug called an HDAC inhibitor. These drugs are usually used to treat cancer and have not been used on Alzheimer's patients. The mice treated with the HDAC inhibitors did better on memory-dependent tasks than the control group. According to Dr. Tsai, more research must be done to understand the effect before this therapy is tried on people. Her team is going to conduct further research to explore how these drugs work.
Both treatments by the MIT team are intriguing, especially because they achieved similar results. The big breakthrough is that memories lost to Alzheimer's disease don't appear to be actually "lost". They still exist in the patient's brain and simply need to be accessed by "regrowing" the neural pathways leading to them. The ability of sick mice to learn new tasks also offers hope to people with advanced Alzheimer's. Even if memories can't be fully recovered, it may be possible to boost their learning capacity and their ability to form new memories. If the study's results are reproduced in human patients, it will go a long way towards turning Alzheimer's into a treatable, manageable illness. Much like some types of cancer, Alzheimer's could one day be, if not curable, a disease that people can live with for a long time and in relative peace and comfort.
Sources
"Scientists 'reverse' memory loss." BBC News. Apr. 29, 2007. http://news.bbc.co.uk/2/hi/health/6606315.stm
"Enhanced Environment Restores Memory in Mice with Neurodegeneration." HHMI News. Apr. 29, 2007. http://www.hhmi.org/news/tsai20070429.html
"Scientists Restore Lost Memory in Alzheimer's-Like Mice." AJC.com. Apr. 29, 2007. http://www.ajc.com/health/content/shared-auto/healthnews/ alzh/604018.html
Peck, Peggy. "Teaching Old Mice New Tricks Opens Doors to Lost Memories." Apr. 30, 2007. Psychiatric Times. http://www.psychiatrictimes.com/psychiatryNews/showArticle.jhtml? articleID=199202782&cid=BreakingN
"What is Alzheimer's?" Alzheimer's Association. http://www.alz.org/alzheimers_disease_what_is_alzheimers.asp
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