Alzheimer's research paper conclusion

Most cases of Alzheimer's disease do not exhibit autosomal-dominant inheritance and are termed sporadic AD, in which environmental and genetic differences may act as risk factors . The best known genetic risk factor is the inheritance of the ε4 allele of the apolipoprotein E (APOE). [45] [46] Between 40 and 80% of people with AD possess at least one APOEε4 allele. [46] The APOEε4 allele increases the risk of the disease by three times in heterozygotes and by 15 times in homozygotes. [40] Like many human diseases, environmental effects and genetic modifiers result in incomplete penetrance . For example, certain Nigerian populations do not show the relationship between dose of APOEε4 and incidence or age-of-onset for Alzheimer's disease seen in other human populations. [47] [48] Early attempts to screen up to 400 candidate genes for association with late-onset sporadic AD (LOAD) resulted in a low yield. [40] [41] More recent genome-wide association studies (GWAS) have found 19 areas in genes that appear to affect the risk. [49] These genes include: CASS4 , CELF1 , FERMT2 , HLA-DRB5 , INPP5D , MEF2C , NME8 , PTK2B , SORL1 , ZCWPW1 , SlC24A4 , CLU , PICALM , CR1 , BIN1 , MS4A , ABCA7 , EPHA1 , and CD2AP . [49]

Alzheimer's research paper conclusion

alzheimer's research paper conclusion

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