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Article type: Review Article
Authors: Korthauer, Laura E.a | Awe, Elizabetha; b | Frahmand, Marijama | Driscoll, Iraa; *
Affiliations: [a] Department of Psychology, University of Wisconsin-Milwaukee, Milwaukee, WI, USA | [b] Department of Neurology, Medical College of Wisconsin, Milwaukee, WI, USA
Correspondence: [*] Correspondence to: Ira Driscoll, PhD, Department of Psychology, 2441 E. Hartford Ave., Milwaukee, WI 53212, USA. Tel.: +1 414 229 6665; driscoli@uwm.edu
Abstract: Alzheimer’s disease (AD) is characterized by memory loss and executive dysfunction, which correspond to structural changes to the medial temporal lobes (MTL) and prefrontal cortex (PFC), respectively. Given the overlap in cognitive deficits between healthy aging and the earliest stages of AD, early detection of AD remains a challenge. The goal of the present study was to study MTL- and PFC-dependent cognitive functioning in middle-aged individuals at genetic risk for AD or cognitive impairment who do not currently manifest any clinical symptoms. Participants (N = 150; aged 40–60 years) underwent genotyping of 47 single nucleotide polymorphisms (SNPs) in six genes previously associated with memory or executive functioning: APOE, SORL1, BDNF, TOMM40, KIBRA, and COMT. They completed two MTL-dependent tasks, the virtual Morris Water Task (vMWT) and transverse patterning discriminations task (TPDT), and the PFC-dependent reversal learning task. Although age was associated with poorer performance on the vMWT and TPDT within this middle-aged sample, there were no genotype-associated differences in cognitive performance. Although the vMWT and TPDT may be sensitive to age-related changes in cognition, carriers of APOE, SORL1, BDNF, TOMM40, KIBRA, and COMT risk alleles do not exhibit alteration in MTL- and PFC-dependent functioning in middle age compared to non-carriers.
Keywords: Aging, Alzheimer’s disease, apolipoproteins E, brain-derived neurotrophic factor, cognition, hippocampus, prefrontal cortex, middle age
DOI: 10.3233/JAD-171043
Journal: Journal of Alzheimer's Disease, vol. 64, no. 2, pp. 459-471, 2018
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