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

## TL;DR

This study explores how brain electrical activity in specific regions can help diagnose Alzheimer's disease using EEG measurements.

## Contribution

The study introduces frontoparietal network topography as a potential diagnostic marker for Alzheimer’s disease using N4/P6 ERPs.

## Key findings

- Controls showed significantly higher N4/P6 peak amplitudes and shorter latencies compared to AD patients.
- N4 ERP appears to be a stronger biomarker than P6 ERP for Alzheimer’s diagnosis.
- FPN integration was observed in healthy controls but not in AD patients during cross-modal tasks.

## Abstract

Numerous prospective biomarkers are being studied for their ability to diagnose various stages of Alzheimer’s disease (AD). High-density electroencephalogram (EEG) methods show promise as an accurate, economical, non-invasive approach to measuring the electrical potentials of brains associated with AD. Event-related potentials (ERPs) may serve as clinically useful biomarkers of AD. Through analysis of secondary data, the present study examined the performance and distribution of N4/P6 ERPs across the frontoparietal network (FPN) using EEG topographic mapping. ERP measures and memory as a function of reaction time (RT) were compared between a group of (n = 63) mild untreated AD patients and a control group of (n = 73) healthy age-matched adults. Based on the literature presented, it was expected that healthy controls would outperform patients in peak amplitude and mean component latency across three parameters of memory when measured at optimal N4 (frontal) and P6 (parietal) locations. It was also predicted that the control group would exhibit neural cohesion through FPN integration during cross-modal tasks, thus demonstrating healthy cognitive functioning consistent with older healthy adults. By targeting select frontal and parietal EEG reference channels based on N4/P6 component time windows and positivity, our findings demonstrated statistically significant group variations between controls and patients in N4/P6 peak amplitudes and latencies during cross-modal testing. Our results also support that the N4 ERP might be stronger than its P6 counterpart as a possible candidate biomarker. We conclude through topographic mapping that FPN integration occurs in healthy controls but is absent in AD patients during cross-modal memory tasks.