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PL‐01‐01: Genetics of Alzheimer's disease: Progress and future
Author(s) -
Haines Jonathan L.
Publication year - 2010
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2010.05.167
Subject(s) - genome wide association study , psen1 , genetic architecture , biology , genetics , genetic association , candidate gene , disease , genetic linkage , apolipoprotein e , gene , alzheimer's disease , computational biology , single nucleotide polymorphism , quantitative trait locus , presenilin , genotype , medicine , pathology
sectional images of the right hippocampus in a normal and AD subject; so, stratum oriens; DG, dentate gyrus; sub, subiculum; scale bar 1 mm). The CA1-SRLM exhibited more thinning than the CA1-SP in AD compared to NC (p 1⁄4 0.003 vs 0.8) (Figure 2: SRLM and SP thickness was measured as illustrated in each individual, averaged over the left and right, and normalized to TIV). Raw, non-normalized measurements revealed the same finding. In addition, hippocampal volume was no different between the groups (p 1⁄4 0.15). Conclusions: Hippocampal CA1 neuropil atrophy, visualized in vivo using 7T MRI, may be a more reliable marker of mild AD than changes in other areas of the hippocampus. These findings validate pathological predictions, possibly providing an objective in vivo biomarker for mild Alzheimer disease.

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