Abstract

Cerebrovascular atherosclerosis has been identified as a prominent pathological feature of Alzheimer’s disease (AD); the link between vessel pathology and AD risk may also extend to extracranial arteries. This study aimed to determine the effectiveness of using arterial pulse-wave measurements and multilayer perceptron (MLP) analysis in distinguishing between AD and control subjects. Radial blood pressure waveform (BPW) and finger photoplethysmography signals were measured noninvasively for 3 min in 87 AD patients and 74 control subjects. The 5-layer MLP algorithm employed evaluated the following 40 harmonic pulse indices: amplitude proportion and its coefficient of variation, and phase angle and its standard deviation. The BPW indices differed significantly between the AD patients (6247 pulses) and control subjects (6626 pulses). Significant intergroup differences were found between mild, moderate, and severe AD (defined by Mini-Mental-State-Examination scores). The hold-out test results indicated an accuracy of 82.86%, a specificity of 92.31%, and a 0.83 AUC of ROC curve when using the MLP-based classification between AD and Control. The identified differences can be partly attributed to AD-induced changes in vascular elastic properties. The present findings may be meaningful in facilitating the development of a noninvasive, rapid, inexpensive, and objective method for detecting and monitoring the AD status.

Highlights

  • Cerebrovascular atherosclerosis has been identified as a prominent pathological feature of Alzheimer’s disease (AD); the link between vessel pathology and AD risk may extend to extracranial arteries

  • The present study found significant differences in several blood pressure waveform (BPW) and PPG indices between AD patients and control subjects

  • The findings of this study and the related conclusions to be drawn can be summarized as follows: 1. Significant differences in BPW and PPG pulse indices were found between the AD patients and control subjects

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Summary

Introduction

Cerebrovascular atherosclerosis has been identified as a prominent pathological feature of Alzheimer’s disease (AD); the link between vessel pathology and AD risk may extend to extracranial arteries. Cerebrovascular atherosclerosis has been identified as a prominent pathological feature of A­ D2 These vascular changes include functional and structural alterations, such as reduced cerebral perfusion and an impaired ability of the cerebral circulation to supply energy substrates and oxygen to active brain r­ egions[2]. These vascular alterations are suggested to play a role in the neuronal dysfunction and damage underlying this type of ­dementia[1]. Presymptomatic individuals at risk of AD exhibit cerebrovascular dysfunction, reduced cerebral blood flow (CBF), and altered permeability of the blood–brain barrier; these raise the possibility that cerebrovascular dysfunction is a presymptomatic correlate of AD p­ athology[1]. With amyloid accumulation reportedly exhibiting profound disruption of neurovascular regulation before the expression of cognitive deficits and amyloid p­ laques[4]

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