• Am J Psychiatry · Nov 2010

    Family history of Alzheimer's disease and hippocampal structure in healthy people.

    • Markus Donix, Alison C Burggren, Nanthia A Suthana, Prabha Siddarth, Arne D Ekstrom, Allison K Krupa, Michael Jones, Laurel Martin-Harris, Linda M Ercoli, Karen J Miller, Gary W Small, and Susan Y Bookheimer.
    • Center for Cognitive Neurosciences, Department of Psychiatry and Biobehavioral Sciences, David Geffen School of Medicine at University of California Los Angeles, Semel Institute, Los Angeles, CA 90095, USA.
    • Am J Psychiatry. 2010 Nov 1; 167 (11): 1399-406.

    ObjectiveStructural brain changes appear years before the onset of Alzheimer's disease, the leading cause of dementia late in life. Determining risk factors for such presymptomatic brain changes may assist in identifying candidates for future prevention treatment trials. In addition to the e4 allele of the apolipoprotein E gene (APOE-4), the major known genetic risk factor, a family history of Alzheimer's disease also increases the risk to develop the disease, reflecting yet unidentified genetic and, perhaps, nongenetic risks. The authors investigated the influence of APOE-4 genotype and family history risks on cortical thickness in medial temporal lobe subregions among volunteers without cognitive impairment.MethodHigh-resolution magnetic resonance imaging (MRI) and a cortical unfolding method were performed on 26 subjects (APOE-4 carriers: N=13; noncarriers: N=13) with at least one first-degree relative with Alzheimer's disease and 25 subjects (APOE-4 carriers: N=12; noncarriers: N=13) without this risk factor. All subjects (mean age: 62.3 years [SD=10.7]; range=38-86 years) were cognitively healthy.ResultsFamily history of Alzheimer's disease and APOE-4 status were associated with a thinner cortex in the entorhinal region, subiculum, and adjacent medial temporal lobe subfields. Although these associations were additive, family history of Alzheimer's disease explained a greater proportion of the unique variance in cortical thickness than APOE-4 carrier status.ConclusionsAPOE-4 carrier status and family history of Alzheimer's disease are independently associated with and contribute additively to hippocampal cortical thinning.

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