Example of alzheimer's research paper

William E. Balch, .
Kristin Baldwin, .
Phil Baran, .
Joel Buxbaum, .
Jerold Chun, ., .
Ronald Davis, .
Sandra Encalada, .
Jeffery Kelly, .
Thomas Kodadek, .
Ian J. MacRae, .
Courtney Miller, .
. Nicolaou, .
Evan Powers, .
Steven Reed, .
Gavin Rumbaugh, .
George Siggins, .
Srinivasa Subramaniam, .
Michael Taffe, .
Luke Wiseman, .
Baoji Xu, .
Xiang-Lei Yang, .

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    As the brain is slowly devoured and gradually succumbs, turning the body into an empty vessel, remembering and writing are more than difficult; they are cold receptacles emptied of content. My memories are slowly disappearing from places inhabited for so long. In themselves, my memories do not compare with the great sagas of this century, the births, deaths, tumult, madness, great art and music, and the intense suffering of so many human beings. Our immortality, such as it may be, is not contained in what we dreamed or the secrets we kept; it is how our friends and loved ones remember us.

    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]

    Example of alzheimer's research paper

    example of alzheimer's research paper

    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]

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