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Andreasen, N., Hesse, C., Davidsson, P., Minthon, L., Wallin, A., Winblad, B., Vanderstichele, H., Vanmechelen, E. and Blennow, K. (1999) Cerebrospinal Fluid β-amyloid(1-42) in Alzheimer Disease. Archives of Neurology, 56, 673-680.
https://doi.org/10.1001/archneur.56.6.673

has been cited by the following article:

• 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.