BACKGROUND AND AIM
Patients with Alzheimer’s disease (AD) indicate impaired driving behaviour and their driving profile is described as conservative, although they maintain the ability to operate a vehicle.1 According to previous research, patients with mild cognitive impairment (MCI) are generally considered safe drivers, however, they also have driving performance deficits.2 Literature regarding the severity of driving impairments in MCI and mild AD has not yet reached a consensus. A recent meta-analysis suggested that the severity of cognitive decline appears to have important predictive utility over driving ability in patients with AD and patients with MCI.3 The apolipoprotein E4 (APOE4) allele, a well-documented genetic risk factor for AD, affects cognition of carriers within the clinical stages of MCI and AD, as reported by studies comparing them with non-carriers. The aim of the current study was to compare the driving behaviour of carriers and non-carriers of APOE4 in the clinical stages of mild AD or amnestic MCI (aMCI).
MATERIALS AND METHODS
Included in the study were 36 active drivers with aMCI or mild AD. Of whom, 18 were carriers of APOE4 and 18 were non-carriers. Each group included 13 aMCI and five mild AD. The two groups had no significant differences in age, years of education, general cognitive ability, and driving experience.
All patients underwent a thorough medical, ophthalmological, neurological, and neuropsychological assessment, and participated in a driving simulation experiment which included a rural environment with low- and high-traffic-volume conditions. Plasma samples were used for APOE genotyping.
RESULTS
The application of independent samples t-test indicated that in high traffic volume, APOE4 carriers had significantly lower average speed (mean [M]= 32.6; standard deviation [SD]= 7.0) than non-carriers (M=38.2; SD=6.1; t[30]=2.40; p=0.023; d=0,85). APOE4 carriers had also lower speed variation (M=7.7; SD=1.5) than non-carriers (M=11.2; SD=2.8; t[30]=4.36; p<0.001; d=0.70). Nonetheless, after the application of the Bonferroni correction the only difference that survived was the measure of speed variation. In low traffic volume there were no significant differences. Regarding the neuropsychological measures, the independent samples t-test detected a significant difference only in the domain of episodic memory. APOE4 carriers had more severe episodic memory disorders (M=5.4; SD=3.3) than non-carriers (M=7.7; SD=2.6; t[27]=2.31; p=0.027; d=0.80). However, this result did not survive after the application of Bonferroni correction.
CONCLUSION
To the authors’ knowledge, this is the first study to investigate the possible effect of APOE4 to driving behaviour. The study found that APOE4 genotype moderates the behaviour of the carriers in a cognitively demanding condition like driving. It should be highlighted that the driving simulator experiment was able to depict a robust significant difference in terms of speed variation despite the absence of significant differences in a variety of neuropsychological measures.
Lower speed variation could sometimes reflect a strategy of compensation that is utilised by drivers in order to avoid driving errors.4 Along this vein, the lower values of the APOE4 carriers could be regarded as a compensatory behaviour for an underlying attentional deficit that was not depicted by the applied neuropsychological measures. Future studies could expand the conclusions of the current study by utilising larger samples as well as by investigating the driving behaviour of APOE4 carriers in preclinical stages.