Treating Alzheimer’s Disease

Alzheimer’s disease is a progressive, irreversible brain disorder. Alzheimer’s disease (AD) is the most common form of dementia among older people. Alzheimer’ destroys a person’s memory and ability to learn, reason, make judgments, communicate and carry out daily activities. Genetic factors are suspected, and dominant mutations in three different genes have been identified that account for a much smaller number of cases of familial, early-onset AD. People with dementia often have trouble thinking and speaking clearly, remembering recent events, and learning new things. Over time, it becomes hard for them to handle everyday activities and take care of themselves. Age is the most important risk factor for AD; the number of people with the disease doubles every 5 years beyond age 65. Three genes have been discovered that cause early onset (familial) AD. Other genetic mutations that cause excessive accumulation of amyloid protein are associated with age-related (sporadic) AD. AD is part of an immune response that is attempting to contain the disease. The former may be more likely, since research indicates that anti-inflammatory drugs can prevent or retard AD development.

Alzheimer’s disease advances at widely different rates. Family history is another risk factor of Alzheimer’s. Several risk factor genes may interact with each other and with non-genetic factors to cause the disease. Cardiovascular Risk Factors The same factors that increase the risk for heart disease and stroke, such as high blood pressure, may also increase the risk for late-onset AD. Most people with mild forgetfulness do not have AD. In the early stage of AD, people may have trouble remembering recent events, activities, or the names of familiar people or things. Oxidative damage refers to cell damage caused by excess free radicals, which are highly reactive chemicals. Free radicals are often formed as a by-product of metabolism, or chemical processes within the cell. Excess free radicals may cause substantial neuronal damage, contributing to AD development. Type 2 Diabetes. A link between AD and type 2 diabetes, the form of diabetes in which insulin levels are high. One theory is that too much insulin in the blood promotes inflammation and oxidative damage in the brain, both of which contribute to AD development.

Symptoms of AD include memory loss, language deterioration, impaired ability to mentally manipulate visual information, poor judgment, confusion, restlessness, and mood swings. Alzheimer’s disease may also include behavioral changes, such as outbursts of violence or excessive passivity in people who have no previous history of such behavior. In the later stages, deterioration of musculature and mobility, leading to bedfastness, inability to feed oneself, and incontinence, will be seen if death from some external cause (e.g. heart attack or pneumonia) does not intervene. Moderate -As the disease progresses to the middle stage, the patient might still be able to perform tasks independently, but may need assistance with more complicated activities. Severe — As the disease progresses from the middle to late stage, the patient will undoubtedly not be able to perform even the simplest of tasks on their own and will need constant supervision. They may even lose the ability to walk or eat without assistance. They might forget to eat and starve.

Treatment Alzheimer’s Disease Tips

1. Acetylcholinesterase (AChE)-inhibitors reduce the rate at which acetylcholine (ACh) is broken down and hence increase the concentration of ACh in the brain (combatting the loss of ACh caused by the death of the cholinergin neurons).

2. Ginkgo for the treatment of “cognitive impairment and dementia,” a Cochrane Review concludes that “there is promising evidence of improvement in cognition and function associated with Ginkgo According to this review the two randomized controlled studies that focused on Alzheimer’s patients both showed significant improvement in these areas.

3. Tramiprosate (3APS or Alzhemed) is a GAG-mimetic molecule that is believed to act by binding to soluble amyloid beta to prevent the accumulation of the toxic plaques.

4. R-flurbiprofen (MPC-7869) is a gamma secretase modulator sometimes called a selective amyloid beta 42 lowering agent. It is believed to reduce the production of the toxic amyloid beta in favor of shorter forms of the peptide.

5. Leuprolide has also been studied for Alzheimer’s. It is hypothesized to work by reducing leutenizing hormone levels which may be causing damage in the brain as one ages.

6. Antihistamine drug Dimebon has also recently been found to show beneficial effects against Alzheimer’s disease in preliminary trials

7. Vaccines or immunotherapy for Alzheimer’s, unlike typical vaccines, would be used to treat diagnosed patients rather than for disease prevention.

8. Proposed alternative treatments for Alzheimer’s include a range of herbal compounds and dietary supplements.

9. Cognitive and behavioral interventions and rehabilitation strategies may be used as an adjunct to pharmacologic treatment, especially in the early to moderately advanced stages of disease.

10. DNA-based therapy is also Treating Alzheimer’s Disease.