Alzheimer’s disease and stem cell therapy part 5

Stem cell 5

 

Familial alzheimer’s disease is caused by gene mutations, and the aggregation of beta-amyloid is observed in familial alzheimer’s disease as a result of a gene mutation of the beta-amyloid precursor protein, which is the main component of senile plaques, one of the hallmark pathological features of alzheimer’s disease. Such excessive beta-amyloid aggregation destroys neurons. Furthermore, there have been reports on the possible link between the apolipoprotein E (APOE) gene and the incidence of alzheimer’s disease. There are three type of APOE, of which E4 is associated with alzheimer’s disease, and E2 and E3 are known to serve the function of providing protection against alzheimer’s disease. Everyone carries APOE gene, and APOE epsilon 4 is the susceptible gene. About 40% of alzheimer’s disease patients are associated with APOE epsilon 4, whereas the remaining 50% or more are known to be not associated with APOE genotype. There are three types of APOE, of which E4 is associated with alzheimer’s diseases, and E2 and E3 are known to serve the function of providing protection against alzheimer’s disease.

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