Driving Behaviour in Alzheimer’s Disease and Amnestic Mild Cognitive Impairment Carriers of the Apolipoprotein E4 Allele - European Medical Journal
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Driving Behaviour in Alzheimer’s Disease and Amnestic Mild Cognitive Impairment Carriers of the Apolipoprotein E4 Allele

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3 Mins
Authors:
Evangelia Stanitsa,1 Ion Beratis,1 Dionysia Kontaxopoulou,1 Stella Fragkiadaki,1 Vicky Papastefanopoulou,2 Dimosthenis Pavlou,3 Panagiotis Papantoniou,3 Christos Kroupis,2 Alexandra Economou,4 John Papatriantafyllou,1 Leonidas Stefanis,5 George Yannis,3 *Sokratis G. Papageorgiou1
Disclosure:

The authors have declared no conflicts of interest.

Acknowledgements:

This paper is based on two research projects implemented within the framework of the Operational Program “Education and Lifelong Learning” of the National Strategic Reference Framework (NSRF), namely the Research Funding Program: THALES. Investing in knowledge society through the European Social Fund, and the Action: ARISTEIA (Action’s Beneficiary: General Secretariat for Research and Technology), co-financed by the European Union (European Social Fund – ESF) and Greek national funds.

Citation
EMJ Neurol. ;8[1]:61-63. Abstract Review No: AR14.

Each article is made available under the terms of the Creative Commons Attribution-Non Commercial 4.0 License.

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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.

References
Papageorgiou SG et al. Does the diagnosis of Alzheimer’s disease imply immediate revocation of a driving license? Int J Clin Neurosci Ment Heal. 2016;3(Suppl 1):S02. Devlin A et al. Investigating driving behaviour of older drivers with mild cognitive impairment using a portable driving simulator. Accid Anal Prev. 2012;49:300-7. Hird MA et al. A Systematic review and meta-analysis of on-road simulator and cognitive driving assessment in Alzheimer’s disease and mild cognitive impairment. J Alzheimer’s Dis. 2016;53(2):713-29. Thompson KR et al. Distracted driving in elderly and middle-aged drivers. Accid Anal Prev. 2012;45:711-7.