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O4–01–03: A common unifying mechanism underlies the amyloid–β and environmental stimulation–related pathological effects of apoE4 in vivo
Author(s) -
Michaelson Daniel M.,
Belinson Haim,
Dolev Iftach,
Levi Ofir,
Ophir Gal
Publication year - 2006
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.2006.05.293
Subject(s) - neurogenesis , stimulation , synaptogenesis , genetically modified mouse , biology , hippocampal formation , hippocampus , neuroscience , neprilysin , transgene , alzheimer's disease , phenotype , amyloid (mycology) , medicine , disease , genetics , biochemistry , botany , gene , enzyme
deactivation pattern of MCI subjects was heterogeneous varying both according to their level of impairment and APOE-4 status. AD patients showed significantly less deactivation than OC in medial parietal and cingulate/retrosplenial cortices (z 5.32, p 0.0001). Comparing OC and AD subgroups, we found evidence of a hierarchy of deactivation decreasing in the following order: OC APOE-4 non-carriers OC APOE-4 carriers AD APOE-4 non-carriers AD APOE-4 carriers. Conclusions: The present study demonstrates that the pattern of task-related fMRI deactivation is remarkably disrupted in AD patients, particularly in AD APOE-4 carriers. Furthermore, consistent with PET findings, APOE-4 was associated with impaired parietal and posterior cingulate deactivation even in cognitively intact older individuals at risk for AD.