Evaluating frontoparietal network topography for diagnostic markers of Alzheimer’s disease

Abstract

AbstractBackgroundA group of mild, untreated AD patients (n = 63) and a control group of healthy age‐matched individuals (n = 73) were compared on amplitudes and latencies of the N4 and P6 ERP.MethodSecondary EEG and behavioral data used for the present study was collected on participants while taking the Alzheimer’s Disease Evoked Potential Test (ADEPT) (Kilborn et al., 2009).ResultWe found a statistically‐significant difference in groups by N4 amplitude [F(1)=32.18, p < 0.001] and N4 latency [F(1)=31.41, p < 0.001], though linear models showed no interaction between these factors. A Tukey HSD post‐hoc test revealed significant pairwise differences between patients and controls (‐0.96 in N4 amplitude and 7.44 in N4 latency). We also found a statistically‐significant difference in groups by P6 amplitude [F(1)=11.12 p < 0.001] and P6 latency [F(1)=11.06, p < 0.001], and linear models showed no interaction between these factors. A Tukey HSD post‐hoc test revealed significant pairwise differences between patients and controls (‐1.13 in P6 amplitude and 7.70 in P6 latency).ConclusionOur results reveal a distinct N4/P6 ERP amplitude attenuation and subsequent component latency increase of mild untreated AD patients during cross‐modal memory tasks, while systematically showing statistically significant group effects in N4/P6 amplitudes and latencies of controls and patients making old/new recognition judgments. Our findings go further to provide evidence that N4 ERP anomalies are potentially more effective than those of their P6 counterpart for use as possible candidate AD biomarkers. Using EEG scalp topography, we visually demonstrate how and approximately where healthy control participants demonstrate neural cohesion through FPN shifting during cross‐modal tasks whereas the AD patients do not.