Alzheimer’s: Genetic Dementia ALZHEIMER’S: Alzheimer’s: Genetic Dementia Essay, Research Paper ALZHEIMER’S: GENETIC DEMENTIA Alzheimer’s, the disease of the degeneration of the brain, was identified in 1907 by German physician Alois Alzheimer. Four million Americans suffer from the disease which deprives the victim of the ability to remember, think, reason, and eventually coordinate movement. This most common form of dementia is caused physically by the gradual change in nerve cells, which leads to the destruction of brain cells. Studies find that this fourth leading cause of death affects more women than men, and more Hispanics and African-Americans than Caucasians. The disease can be present in two forms; early onset Alzheimer’s affects those younger than age 65, whereas late onset Alzheimer’s affects those older.
Late onset Alzheimer’s affects more than 90 % of sufferers. This more common form has been recently discovered to affect those who possess a certain allele of the APOE, apolipoprotein E, gene located on Chromosome 19. APOE, which encodes a protein that helps transport cholesterol in the body and also is involved in nerve cell repair, comes in three alleles, e 2, e 3, and e 4. Those with one or two e 4 alleles are deemed at higher risk of Alzheimer’s disease, although those who possess APOE-e 4 are not guaranteed to develop the disease. APOE-e 4 may simply be unable to efficiently repair nerve cells. The presence of e 4 does not signify if person will develop Alzheimer’s; instead, it signifies when he or she will get it.
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Recent studies suggest that Alzheimer’s may be affected by an interaction between APOE and the newly discovered risk factor alpha-2-macrogobulin, A 2 M, a gene mutation on chromosome 12. A 2 M is a protein that deactivates proteases, enzymes that carve up other proteins. Alpha-2-macrogobulin’s involvement in Alzheimer’s development is especially likely because it attaches to the same cell surface protein as APOE and amyloid precursor-protein (APP).
The un mutated form of A 2 M helps to get rid of the APP fragment beta-amyloid, which is present in excess amounts in the brains of Alzheimer’s patients. The mutant A 2 M, which does not properly remove protein, but only makes the aging brain vulnerable; it does not guarantee affliction. Another possible genetic risk factor for Alzheimer’s disease is the presence of the bleomycin hydrolase gene, which comes in the two alleles A and G.
People who have two G alleles and no APOE-e 4 are also susceptible to the disease. The purpose of bleomycin hydrolase is unknown other than its function to detoxify bleomycin, a common cancer drug. Researchers are also debating the possibility of the HLA gene playing a role in the onset of Alzheimer’s. Early-onset familial Alzheimer’s affects somewhere between one to ten percent of all Alzheimer’s sufferers. One family of German descendants who settled in the Volga Valley contains dozens of members who developed Alzheimer’s at middle age. Genes for this version have been identified on chromosomes 1, 14, and 21.
The chromosome 21 gene carries the code for a mutated form of the amyloid precursor protein, APP, the parent protein for beta amyloid. Also, a variation of the gene that regulates the immune system seems to be the base cause of early onset Alzheimer’s. The common for of human leukocyte antigen, or HLA, determines when Alzheimer’s patients begin to exhibit symptoms of the disease. The HLA-A 2 allele, or a gene close to it, could possibly be the factor that determines when a person begins to exhibit Alzheimer’s. Those who have the A 2 allele of the gene form symptoms an average of three years earlier than those who lack it. Those who retain both the A 2 allele of the HLA gene and two APOE-e 4 genes acquire Alzheimer’s about 10 years before those who have neither.
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The knowledge that HLA-A 2 plays an important role in governing the immune system supports the theory that an immune or inflammatory mechanism plays a significant part in the development of Alzheimer’s. Speculation exists as to whether the immune system attacks its own brain tissue. This rationale is also supported by the fact that those at risk have been able to make some preventive use of anti-inflammatory drugs such as ibuprofen. Other risk factors contribute to the onset of Alzheimer’s disease. Children of Alzheimer’s patients face a 50% chance of having it too. Women are about 50 percent more likely to develop Alzheimer’s than men; however, they also have available to them the preventive measure of postmenopausal hormone replacement therapy.
Estrogen has proven to have a protective effect against Alzheimer’s; it preserves, or possibly even stimulates, the production of acetylcholine, the chemical which helps message transmission. Furthermore, studies have shown that Alzheimer’s is less common among highly educated or very mentally active older people. Those afflicted by Down syndrome, if they survive into their forties, also develop Alzheimer’s, probably because of the extra version of chromosome 21; they too have tangles and plaques form in their brains. Risk of Alzheimer’s doubles each decade past the age of 65.
Approximately 40 % of all those who grow old develop the disease. This type of dementia proceeds in stages, gradually destroying memory, reason, judgment, language, and eventually the ability to carry out even the simplest of tasks. Those who suffer from it face paranoia, suspicion, inability to control emotions and behavior, and incapability to adapt to simple changes or to solve problems. Eventually, all physical functioning becomes impossible; immobility prevails, to be followed by death.
... Mycophenolate mofetil Mycophenolate Mofetil (MM) is a newly developed immunosuppressant which has been proven to be promising in the ... amp; IMMUNOMODULATION By providing an overview of the adaptive immune responses it becomes apparent that two areas of pharmacological ... weaken the patients defence mechanism and therefore increase the risk of infection by opportunistic pathogens (Downie et. al., ...