New Information on Alzheimer's Disease
Alzheimer's disease is the most common cause of dementia. It is an irreversible progressive brain disease that slowly destroys brain cells, destroying memory and thinking skills and eventually the ability to carry out the simplest of tasks. The incidence of Alzheimer's is rising, however, beyond treating merely the symptoms, treatment of the underlying causes are beginning to be addressed by researchers. Find out the latest information on, causes, prevalence, current treatments and new treatment strategies that are on the horizon.
What causes Alzheimer's disease?
Although how the disease starts it is still unknown, we do know that damage to the brain begins as early as 10 to 20 years before problems are evident. This occurs in the formation of abnormal clumps (amyloid plaques) and tangled bundles of fibers (neurofibrillary tangles). As plaques and tangles form, healthy neurons lose their ability to function, and eventually they die. This damaging process spreads to the hippocampus, a nearby structure that is essential for forming memories. As the death of neurons increases, affected brain regions begin to shrink. By the final stage of Alzheimer's, damage is widespread and brain tissue has shrunk significantly.
It is likely that over a long period of time, age-related changes, genetic, environmental, and lifestyle factors occur and contribute to disease progression.
1. Age-related changes in the brain include atrophy (shrinking) of certain parts of the brain, inflammation, and the production of unstable molecules called free radicals which harm neurons.
2.Genetics - people who develop Alzheimer's before age 65 usually have a mutation, or permanent change, in one of three inherited genes located on chromosomes 1 (SEN2), 14 (SEN1) and 21 (APP, A4). These gene mutations cause "early-onset" disease, however, not all early-onset cases are caused by these mutations.
Most people have "late-onset" disease, which usually develops after age 65, and is linked to the gene APOE. Having the APOE e4 form of APOE, increases a person's risk of getting Alzheimer's. Forty percent of all people who develop late-onset Alzheimer's carry APOE e4. However, carrying APOE e4 does not always mean that a person will develop Alzheimer's, and people carrying no APOE e4 forms can still develop the disease.
Additional genes may influence the development of late-onset disease. Scientists have identified variants of the SORL1, CLU, PICALM, and CR1 genes that may play a role in risk of late-onset Alzheimer's.
3. Lifestyle factors -new research suggests that a nutritious diet, physical activity, social engagement, and mentally stimulating activities can all help to reduce the risk of cognitive decline and Alzheimer's Disease. Scientists are now investigating associations between cognitive decline and vascular and metabolic conditions such as heart disease, stroke, high blood pressure, diabetes, and obesity to determine whether reducing risk factors for these diseases may help with Alzheimer's.
New information on Alzheimer's Disease as of 2010
As stated by the Alzheimer's Association report of 2010, new information on several aspects of the disease is evident:
1. Prevelance
times more likely than whites to have dementia. This may be related to incidence
of high blood pressure, diabetes, low socio economic status and education.
2. Current treatment - the U.S. Food and Drug Administration (FDA) has approved
five medications to treat the symptoms of Alzheimer's disease by disease stage.
3. Future treatments-three separate clinical trails are beginning, to determine future
diagnosis and treatment of Alzheimer's Disease.
where symptoms and impairment are milder.
reduce the presence of amyloid plaques.
Obtain more helpful suggestions for personal growth and security by visiting the author's information.
What causes Alzheimer's disease?
Although how the disease starts it is still unknown, we do know that damage to the brain begins as early as 10 to 20 years before problems are evident. This occurs in the formation of abnormal clumps (amyloid plaques) and tangled bundles of fibers (neurofibrillary tangles). As plaques and tangles form, healthy neurons lose their ability to function, and eventually they die. This damaging process spreads to the hippocampus, a nearby structure that is essential for forming memories. As the death of neurons increases, affected brain regions begin to shrink. By the final stage of Alzheimer's, damage is widespread and brain tissue has shrunk significantly.
It is likely that over a long period of time, age-related changes, genetic, environmental, and lifestyle factors occur and contribute to disease progression.
1. Age-related changes in the brain include atrophy (shrinking) of certain parts of the brain, inflammation, and the production of unstable molecules called free radicals which harm neurons.
2.Genetics - people who develop Alzheimer's before age 65 usually have a mutation, or permanent change, in one of three inherited genes located on chromosomes 1 (SEN2), 14 (SEN1) and 21 (APP, A4). These gene mutations cause "early-onset" disease, however, not all early-onset cases are caused by these mutations.
Most people have "late-onset" disease, which usually develops after age 65, and is linked to the gene APOE. Having the APOE e4 form of APOE, increases a person's risk of getting Alzheimer's. Forty percent of all people who develop late-onset Alzheimer's carry APOE e4. However, carrying APOE e4 does not always mean that a person will develop Alzheimer's, and people carrying no APOE e4 forms can still develop the disease.
Additional genes may influence the development of late-onset disease. Scientists have identified variants of the SORL1, CLU, PICALM, and CR1 genes that may play a role in risk of late-onset Alzheimer's.
3. Lifestyle factors -new research suggests that a nutritious diet, physical activity, social engagement, and mentally stimulating activities can all help to reduce the risk of cognitive decline and Alzheimer's Disease. Scientists are now investigating associations between cognitive decline and vascular and metabolic conditions such as heart disease, stroke, high blood pressure, diabetes, and obesity to determine whether reducing risk factors for these diseases may help with Alzheimer's.
New information on Alzheimer's Disease as of 2010
As stated by the Alzheimer's Association report of 2010, new information on several aspects of the disease is evident:
1. Prevelance
- 5.3 million Americans have Alzheimer's disease and 5.1 of these are over age 65. That is 1 in 8 people over the age of 65.
- More women have the disease than men, primarily because women live longer than men.
- Less education is associated with a higher risk of developing dementia, possibly due to less cognitive reserve, a lower socio-economic status, and poorer medical care.
- African Americans are two times and Hispanics are one and one half
times more likely than whites to have dementia. This may be related to incidence
of high blood pressure, diabetes, low socio economic status and education.
2. Current treatment - the U.S. Food and Drug Administration (FDA) has approved
five medications to treat the symptoms of Alzheimer's disease by disease stage.
- Donepezil (Aricept) for all stages.
- Galatamine (Razadyne), Rivastigmine (Exelon), and Tacrine (Cognex) for mild to moderate stages.
- Memantine (Namenda) for moderate to severe stages.
3. Future treatments-three separate clinical trails are beginning, to determine future
diagnosis and treatment of Alzheimer's Disease.
- Better diagnosis -using biomarker s to identify disease at a very early stage
where symptoms and impairment are milder.
- Immunoglobulin Treatment–Using intravenous immunoglobulin IGIv, to
reduce the presence of amyloid plaques.
- Treatment with Ceregene's CERE-110 - , a gene therapy product designed to deliver nerve growth factor (NGF) to the brain for the treatment.
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