Mild cognitive impairment vs. mild cognitive dysfunctions: validation with a nomothetic network approach

Michael Maes,Sookjaroen Tangwongchai

doi:10.20517/and.2021.08

Michael Maes, Sookjaroen Tangwongchai

Open Access

https://doi.org/10.20517/and.2021.08

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Abstract

Mild cognitive impairment vs. mild cognitive dysfunctions: validation with a nomothetic network approach

Highlights

Alzheimer’s disease (AD), the major cause of dementia, is a progressive brain disorder characterized by neuroinflammatory and neurodegenerative processes[1,2,3,4]
People with mild cognitive dysfunctions (MCD) show OBD and BIORISK scores that are significantly different from controls and AD
The aims of the present study were: (1) to define the paths from biomarkers (ApoE4, fasting blood glucose (FBG), folate, atherogenic index of plasma (AIP), albumin, hypertension, and diabetes) and their interactions to the cognitome and phenome of amnestic mild cognitive impairment (aMCI) and AD; and (2) to define and validate the subgroup of aMCI patients who take up an intermediate position between controls and AD patients with respect to cognitive, behavioral, social and biomarker data

Summary

Introduction

Alzheimer’s disease (AD), the major cause of dementia, is a progressive brain disorder characterized by neuroinflammatory and neurodegenerative processes[1,2,3,4]. Around 40% of AD patients carry the ApoE4 allele, and the risk of AD is increased in E2/E4 (odds ratio = 2.6), E3/E4 (odds ratio = 3.2), and especially E4/E4 (odds ratio = 14.9) carriers[10] These ApoE genotypes impact the delivery of lipids to cells and amyloid-β deposits and are associated with increased oxidative stress in the brain and a proinflammatory glial response to inflammatory stimuli[11,12], which play a role in synaptic dysfunctions, neuroinflammation, and neurodegeneration[9,12]. Interactions between the presence of the E4 allele and fasting blood glucose (FBG) and albumin and the cumulative effects of the E4 allele with folic acid, glucose, albumin, and the atherogenic index of plasma (AIP) may increase cognitive deficits in memory and naming and the symptomatic burden in AD[6,13] Both hypertension and T2DM may increase risk of AD through immune and oxidative stress-associated mechanisms[14,15,16,17]. No studies have examined whether interactions among those biomarkers, hypertension, and T2DM may impact the neurocognitive as well as behavioral and social dysfunctions in AD

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