Effects of risk genes on BOLD activation in presymptomatic carriers of familial alzheimer's disease mutations during a novelty encoding task

dc.contributorRingman, J.M., Department of Neurology, David Geffen School of Medicine, University of California at Los Angeles, 10911 Weyburn Avenue, #200, Los Angeles, CA 90095-7226, United States; Medina, L.D., Department of Neurology, David Geffen School of Medicine, University of California at Los Angeles, 10911 Weyburn Avenue, #200, Los Angeles, CA 90095-7226, United States; Braskie, M., Department of Neurology, David Geffen School of Medicine, University of California at Los Angeles, 10911 Weyburn Avenue, #200, Los Angeles, CA 90095-7226, United States, Semel Institute for Psychiatry and Human Behavior, University of California at Los Angeles, Los Angeles, CA 90095, United States; Rodriguez-Agudelo, Y., Laboratory of Experimental Psychology, National Institute of Neurology and Neurosurgery, Mexico City 14269, Mexico; Geschwind, D.H., Department of Neurology, David Geffen School of Medicine, University of California at Los Angeles, 10911 Weyburn Avenue, #200, Los Angeles, CA 90095-7226, United States; MacIas-Islas, M.A., Department of Neuroscience, University of Guadalajara, Guadalajara 44130, Mexico; Cummings, J.L., Department of Neurology, David Geffen School of Medicine, University of California at Los Angeles, 10911 Weyburn Avenue, #200, Los Angeles, CA 90095-7226, United States; Bookheimer, S., Semel Institute for Psychiatry and Human Behavior, University of California at Los Angeles, Los Angeles, CA 90095, United States
dc.creatorRingman, J.M.
dc.creatorMedina, L.D.
dc.creatorBraskie, M.
dc.creatorRodriguez-Agudelo, Y.
dc.creatorGeschwind, D.H.
dc.creatorMacIas-Islas, M.A.
dc.creatorCummings, J.L.
dc.creatorBookheimer, S.
dc.date.accessioned2015-09-15T17:51:27Z
dc.date.accessioned2022-11-02T16:33:25Z
dc.date.available2015-09-15T17:51:27Z
dc.date.available2022-11-02T16:33:25Z
dc.date.created2015-09-15T17:51:27Z
dc.date.issued2011
dc.identifierhttp://hdl.handle.net/20.500.12104/41133
dc.identifierhttp://www.scopus.com/inward/record.url?eid=2-s2.0-79952830370&partnerID=40&md5=12232d377ac07130195b9fa35da9f14b
dc.identifier10.1093/cercor/bhq158
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/5022622
dc.description.abstractPrior functional magnetic resonance imaging (fMRI) studies have found increased activity-related blood oxygen level-dependent (BOLD) signal in cognitively normal persons at genetic risk for Alzheimer's disease (AD). This has been interpreted as a compensatory response to incipient AD pathology. We studied the effects of fully penetrant familial Alzheimer's disease (FAD) mutations and apolipoprotein E (APOE) genotype on BOLD fMRI during a novelty encoding task in presymptomatic subjects. Twenty-three Mexican or Mexican-American persons at-risk for inheriting FAD mutations performed a block design novelty encoding task, and activation exhibited by FAD mutation carriers (MCs) was contrasted with that of noncarriers (NCs) and among APOE genotype groups. FAD MCs (n = 14) showed decreased BOLD activation in the anterior cingulate gyrus relative to 9 NCs. No increased activation was seen in MCs relative to NCs. Four APOE ?3/4 carriers demonstrated increased BOLD signal compared with 14 ?3/3 carriers in the occipital and perisylvian cortices bilaterally. There were no areas where ?3/3 carriers activated more than ?3/4 carriers. Our findings of increased fMRI activation associated with APOE genotype but not with FAD mutations suggest that APOE exerts an effect on the BOLD signal that is not readily explained as a compensatory phenomenon. Zapotitlán 2011 The Author. Published by Oxford University Press. All rights reserved.
dc.relationScopus
dc.relationWOS
dc.relationCerebral Cortex
dc.relation21
dc.relation4
dc.relation877
dc.relation883
dc.titleEffects of risk genes on BOLD activation in presymptomatic carriers of familial alzheimer's disease mutations during a novelty encoding task
dc.typeArticle


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