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Details

Autor(en) / Beteiligte
Titel
Role of family history for Alzheimer biomarker abnormalities in the adult children study
Ist Teil von
  • Archives of neurology (Chicago), 2011-10, Vol.68 (10), p.1313
Ort / Verlag
United States
Erscheinungsjahr
2011
Quelle
MEDLINE
Beschreibungen/Notizen
  • To assess whether family history (FH) of Alzheimer disease (AD) alone influences AD biomarker abnormalities. Adult Children Study. Washington University's Charles F. and Joanne Knight Alzheimer's Disease Research Center. A total of 269 cognitively normal middle- to older-aged individuals with and without an FH for AD. Clinical and cognitive measures, magnetic resonance imaging-based brain volumes, diffusion tensor imaging-based white matter microstructure, cerebrospinal fluid biomarkers, and molecular imaging of cerebral fibrillar amyloid with positron emission tomography using the [(11)C] benzothiazole tracer, Pittsburgh compound B. A positive FH for AD was associated with an age-related decrease of cerebrospinal fluid Aβ42; the ε4 allele of apolipoprotein E (APOE4) did not alter this effect. Age-adjusted cerebrospinal fluid Aβ42 was decreased for individuals with APOE4 compared with the level for those without, and the decrease was larger for individuals with a positive FH compared with the decrease for those without. The variation of cerebrospinal fluid tau and Pittsburgh compound B mean cortical binding potential increased by age. For individuals younger than 55, an age-related increase in mean cortical binding potential was associated with APOE4 but not FH. For individuals older than 55, a positive FH and a positive APOE4 implied the fastest age-related increase in mean cortical binding potential. A positive FH was associated with decreased fractional anisotropy from diffusion tensor imaging in the genu and splenium of the corpus callosum. Independent of APOE4, FH is associated with age-related change of several cerebrospinal fluid, Pittsburgh compound B, and diffusion tensor imaging biomarkers in cognitively normal middle- to older-aged individuals, suggesting that non- APOE susceptibility genes for AD influence AD biomarkers.

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