Affiliations: [a] Universidad Nacional del Sur (UNS), Bahía Blanca, Argentina, Instituto de Investigaciones en Ingeniería Eléctrica (IIIE) (UNS-CONICET), Bahía Blanca, Buenos Aires, Argentina
| [b] Clínica Privada Bahiense, Bahía Blanca, Buenos Aires, Argentina
| [c] Department of Psychology, School of Social Sciences, Heriot-Watt University, Edinburgh, UK
| [d] Universidad Autónoma del Caribe, Facultad de Psicología, Barranquilla, Colombia
Correspondence:
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Correspondence to: Gerardo Fernández, IIIE – San Andrés 800, 8000 Bahía Blanca, Buenos Aires, Argentina. Tel.: +54 291 45951801, ext. 3321; E-mail: [email protected].
Abstract: Patients with Alzheimer’s disease (AD) typically present with attentional and oculomotor abnormalities that can have an impact on visual processing and associated cognitive functions. Over the last few years, we have witnessed a shift toward the analyses of eye movement behaviors as a means to further our understanding of the pathophysiology of common disorders such as AD. However, little work has been done to unveil the link between eye moment abnormalities and poor performance on cognitive tasks known to be markers for AD patients, such as the short-term memory-binding task. We analyzed eye movement fixation behaviors of thirteen healthy older adults (Controls) and thirteen patients with probable mild AD while they performed the visual short-term memory binding task. The short-term memory binding task asks participants to detect changes across two consecutive arrays of two bicolored object whose features (i.e., colors) have to be remembered separately (i.e., Unbound Colors), or combined within integrated objects (i.e., Bound Colors). Patients with mild AD showed the well-known pattern of selective memory binding impairments. This was accompanied by significant impairments in their eye movements only when they processed Bound Colors. Patients with mild AD remarkably decreased their mean gaze duration during the encoding of color-color bindings. These findings open new windows of research into the pathophysiological mechanisms of memory deficits in AD patients and the link between its phenotypic expressions (i.e., oculomotor and cognitive disorders). We discuss these findings considering current trends regarding clinical assessment, neural correlates, and potential avenues for robust biomarkers.
