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Chartier-Harlin, M.C., Parfitt, M., Legrain, S., Pérez-Tur, J., Brousseau, T., Evans, A., Berr, C., Vidal, O., Roques, P., Gourlet, V., Fruchart, J.C., Delacourte, A., Rossor, M. and Amouyel, P. (1994) Apolipoprotein E, ε4 Allele as a Major Risk Factor for Sporadic Early and Late-Onset Forms of Alzheimer’s Disease: Analysis of the 19q13.2 Chromosomal Region. Human Molecular Genetics, 3, 569-574.
https://doi.org/10.1093/hmg/3.4.569
has been cited by the following article:
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TITLE:
Early-Onset Alzheimer’s Disease and Metabolic Dysfunction, a Comparative Review
AUTHORS:
Julie Anne Griffith, Marie Kelly-Worden
KEYWORDS:
Alzheimer’s Disease, Early-Onset, Late-Onset, Glucose Metabolism
JOURNAL NAME:
Advances in Alzheimer's Disease,
Vol.7 No.1,
March
30,
2018
ABSTRACT: Alzheimer’s disease is quickly becoming one of the most
known diseases in the country due to its devastating effects and lack of
treatment options. Within this lethal disease, there is a smaller group, those
individuals that are diagnosed with early-onset Alzheimer’s disease. It is
understood that these individuals see faster effects of the disease and die
considerably sooner, but it is not understood why. This review compares the
early-onset (EOAD) and late-onset (LOAD) types to try and determine some of the
most blaring differences between the two. The genetic basis linking EOAD and
LOAD has been the apolipoprotein E gene (APOE) to indicate metabolic alteration
with the ε4 allele specifically.
The topographical atrophy disparities between EOAD and LOAD supported the more
noticeable cognitive differences between the two Alzheimer’s disease
categories. The faster and wider spread atrophy of EOAD patients correlates
with the difficulty they experience with attention, language, visuo-spatial,
and executive functions. Finally, brain metabolism
differs between both AD subtypes as well, where EOAD indicates the wide spread
damage and metabolic breakdown across more diverse regions of the brain.
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