AUTHOR=Gao Lijuan , Chen Jiu , Gu Lihua , Shu Hao , Wang Zan , Liu Duan , Yan Yanna , Zhang Zhijun 

TITLE=Effects of Gender and Apolipoprotein E on Novelty MMN and P3a in Healthy Elderly and Amnestic Mild Cognitive Impairment

JOURNAL=Frontiers in Aging Neuroscience

VOLUME=10

YEAR=2018

URL=https://www.frontiersin.org/journals/aging-neuroscience/articles/10.3389/fnagi.2018.00256

DOI=10.3389/fnagi.2018.00256

ISSN=1663-4365

ABSTRACT=<p><bold>Background:</bold> The apolipoprotein E epsilon4 (<italic>ApoE</italic> ε4) allele and female gender may be important risk factors for the development of Alzheimer’s disease and amnestic mild cognitive impairment (aMCI). Novelty mismatch negativity (MMN) represents the pre-attentive index of deviance detection and P3a represents the attention orienting response. Furthermore, MMN and P3a components have been reported to be potential markers in aMCI. Therefore, this study will investigate the effects of gender and <italic>ApoE</italic> on auditory novelty MMN and P3a and their relationship to neuropsychological performance in aMCI.</p><p><bold>Methods:</bold> Thirty nine aMCI subjects and 44 controls underwent neuropsychological assessment and <italic>ApoE</italic> genotyping. Novelty MMN and P3a components were investigated during an auditory novelty oddball task.</p><p><bold>Results:</bold> Firstly, novelty MMN latency was significantly shorter in aMCI than in healthy control (HC) group. Secondly, novelty MMN latency was negatively correlated with episodic memory in aMCI, but not in HC. Novelty P3a latency was negatively correlated with information processing speed in all subjects. For gender effect, novelty MMN latency was shorter in aMCI females than in HC females. Moreover, novelty P3a amplitudes were lower in males than in females in both aMCI and HC. For the effect of <italic>ApoE</italic> status, novelty MMN latency was shorter in aMCI <italic>ApoE</italic> ε4- than HC <italic>ApoE</italic> ε4-.</p><p><bold>Conclusion:</bold> aMCI presents altered pre-attentive processing indexed by novelty MMN components. Furthermore, there may be a compensatory mechanism on the impaired processing in aMCI. It further suggests that aMCI female and <italic>ApoE</italic> ε4- recruited the compensatory mechanism.</p>