Subjective cognitive impairment: increased prefrontal cortex activation compared to controls during an encoding task

被引:73
作者
Rodda, Joanne E.
Dannhauser, Thomas M.
Cutinha, Darren J.
Shergill, Sukhwinder S. [1 ,2 ]
Walker, Zuzana
机构
[1] UCL, Inst Neurol, Wellcome Dept Imaging Sci, London WC1E 6BT, England
[2] Kings Coll London, Inst Psychiat, London, England
基金
英国惠康基金;
关键词
Subjective cognitive impairment; memory complaints; Alzheimer's disease; fMRI; encoding; mild cognitive impairment; MEMORY COMPLAINTS; ALZHEIMERS-DISEASE; BRAIN ACTIVATION; HIPPOCAMPAL ACTIVATION; APOE GENOTYPE; OLDER-ADULTS; FMRI; RISK; COMMUNITY; DEMENTIA;
D O I
10.1002/gps.2207
中图分类号
R592 [老年病学]; C [社会科学总论];
学科分类号
03 ; 0303 ; 100203 ;
摘要
Objective Subjective cognitive impairment (SCI) has been proposed as a clinical stage which may precede mild cognitive impairment in the clinical continuum of AD, and is characterised by the presence of subjective memory complaints in the absence of objective cognitive deficits. Specific memory-related brain activation differences have been reported in mild cognitive impairment and in cognitively normal individuals at known genetic risk of AD; our objective was to determine whether similar differences are present in people with SCI. Methods We compared brain activation in a memory clinic sample of 10 SCI Subjects and 10 controls during a verbal episodic memory encoding task using functional magnetic resonance imaging (fMRI). Results There were no differences between groups on measures of encoding success (recognition accuracy) nor was there evidence of altered semantic processing. Both groups activated left prefrontal cortex (PFC) and cerebellum during encoding. The SCI group also demonstrated activation in left medial temporal, occipitoparietal and medial frontal cortex. Group comparisons revealed increased activation in SCI in left PFC, where activation strength correlated with memory task performance. Conclusions The activation differences reported in this Study may reflect the employment of compensatory strategies in the face of early AD pathology, although a number of alternative explanations need to be considered. Further studies with larger samples may help to determine whether the observed activation changes are likely to be associated with early neuropathological processes or with other unrelated factors. Copyright (C) 2009 John Wiley & Sons, Ltd.
引用
收藏
页码:865 / 874
页数:10
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