The interplay of neurotransmitters in Alzheimer's disease.
Clinical Application: Acetylcholine and Alzheimer's Disease As hippocampal cells lose their connection to other neurons and die, short-term memory falters. The cholinergic hypothesis of Alzheimer's disease: a review of progress Such studies have resulted in the discovery of an association between a decline in. The pathogenesis of Alzheimer's disease (AD) has been linked to a to the relationship between acetylcholine dysfunction and AD have been.
Interestingly, doctors have found some people who showed no symptoms of Alzheimer's Disease and still had a significant number of plaques and tangles in their brains at autopsy.
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These people may have developed a so called "cognitive reserve," or a large number of connections between brain cells due to healthy lifestyle habits discussed later and a high level of education which acted like a "buffer" to stave off the symptoms of the disease. Another theory is that plaques and tangles begin to form several years before Alzheimer's symptoms actually appear, so people who have plaques and tangles but no signs of AD may have died of another cause before living long enough to become cognitively impaired.
Because of this mystery why some people with large amounts of plaques and tangles don't have AD symptomsmany scientists believe there is more to Alzheimer's Disease than abnormal protein accumulations, although these do seem to play a significant role in the development of the disease.
The AD Brain - Free Radicals Individuals with Alzheimer's Disease seem to have double the amount of destruction created by free radicals in the frontal and temporal side portions of the brain when compared to people aging normally. Both of these brain areas are important for memory and other advanced cognitive functions. The AD Brain - Neurotransmitters Neurotransmitters are chemicals that carry messages between neurons so that the cells can function properly. If the brain produces too much or too little of a particular neurotransmitter, problems such as memory impairment, confusion, or depression can occur.
While most scientists do not think that changes in neurotransmitter levels cause AD, neurotransmitter levels are affected by the illness and contribute to the thinking problems that accompany it.
Several medications used to treat symptoms of Alzheimer's Disease target neurotransmitters, which provides indirect evidence that these brain chemicals are somehow involved. Two neurotransmitters seem to play a role in Alzheimer's Disease: Acetylcholine ACh activates muscles and helps with arousal, short-term memory, and learning. Where they occur determines the seriousness of the problem and the nature of the symptoms.
Symptoms that begin suddenly may be a sign of this kind of dementia. But it differs from both Alzheimer's and normal age-related memory change. People with MCI have ongoing memory problems, but do not experience confusion, attention problems, and difficulty with language. Treating Alzheimer's No treatment so far stops Alzheimer's.
Also, some medicines may help control sleeplessness, agitation, wandering, anxiety, and depression.
Treating these behavioral symptoms often comforts patients and eases their care. Five prescription drugs currently are approved by the U. Food and Drug Administration to treat people with Alzheimer's disease. Although patients can achieve comfort, dignity, and independence for longer periods, and caregiving can be less difficult, it is important to remember that none of these medications stops the disease itself.
They are Razadyne galantamineExelon rivastigmineAricept donepeziland Cognex tacrine. They are known as cholinesterase inhibitors.
The interplay of neurotransmitters in Alzheimer's disease.
Scientists believe they prevent the breakdown of acetylcholine, a brain chemical that may be important for memory, and may help to delay or prevent the symptoms of Alzheimer's from becoming worse for a limited time. As Alzheimer's progresses, the brain produces less and less acetylcholine; therefore, cholinesterase inhibitors may eventually lose their effect. Namenda's main effect is to delay progression of some of the symptoms of moderate to severe Alzheimer's.
Patients may be able to maintain certain daily functions a little longer, such as going to the bathroom independently for several more months, benefiting themselves and their caregivers. Scientists believe that Namenda works by regulating glutamate, another important brain chemical that, when produced in excessive amounts, may lead to brain cell death. Because Namenda works very differently from cholinesterase inhibitors, the two types of drugs can be prescribed in combination.
Compared with those on the placebo, the study group taking donepezil was found to be at reduced risk of progressing to AD for the first 18 months of the three year study.
However, the reduced risk disappeared after 18 months, and by the end of the study, the probability of the two groups progressing to AD was the same.
Neuroimaging Damage to parts of the brain involved in memory, such as the hippocampus, can sometimes be seen on brain scans before symptoms of AD occur. Information may also be requested through the study's Web site: Inflammation Evidence shows that inflammation in the brain may contribute to AD damage. Some studies have suggested that drugs such as nonsteroidal antiinflammatory drugs NSAIDs might help slow AD, but clinical trials thus far have not demonstrated a benefit from these drugs.
Antioxidants Several years ago, a clinical trial showed that vitamin E slowed the progress of some consequences of AD by about seven months. Additional studies are investigating whether antioxidants—vitamins E and C—can, too.
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Ginkgo biloba Early studies suggested that extracts from the leaves of the ginkgo biloba tree may help treat AD symptoms. There is no evidence yet that ginkgo biloba will cure or prevent AD, but scientists now are trying to find out in a clinical trial whether it can delay cognitive decline or prevent dementia in older people.
To Find Out More Visit www. However, clinical trials have not shown that it can slow the progression of already diagnosed AD. And one study found that women over the age of 65 who used estrogen with a progestin were at greater risk of dementia, including AD, and that older women using only estrogen could also increase their chance of developing dementia.
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