Abstract

Amnestic mild cognitive impairment (aMCI) is a sub-clinical condition characterized by memory deficits that are not severe enough to affect daily functioning. Here we investigated two potential biomarkers found in the cerebrospinal fluid of AD patients, APLP1-derived Aβ-like peptides 28 (APL1β28) and clusterin plasma levels, in terms of their relationship to cognitive function, as reflected in the Mini-Mental State Examination (MMSE), the Montreal Cognitive Assessment (MoCA) and the Cognitive Assessment Screening Instrument (CASI) in aMCI patients. Forty-seven aMCI patients and thirty-five age- and gender-matched healthy adult controls were recruited for this study. Using the ELISA method, we found that the mean concentrations of both APL1β28 and clusterin were not significantly different between the control and aMCI groups. The APL1β28 levels were positively correlated with clusterin and that both were negatively correlated with the MMSE scores of the aMCI patients. Clusterin levels were negatively correlated with the MoCA and CASI scores of the aMCI patients. Using multivariate analysis, the correlation between clusterin and MMSE/MoCA/CASI was independent of other AD risk factors including age, education, sex, body mass index and ApoE genotype. The data presented here demonstrate that plasma clusterin levels reflect cognitive function in aMCI patients.

Highlights

  • Amnestic mild cognitive impairment, which affects 5–6% of people older than 65, is a syndrome attributed to people with noticeable impairments in memory function but whose other cognitive functions are normal[1,2,3,4,5,6,7,8]

  • These results indicate that Amnestic mild cognitive impairment (aMCI) patients with higher APL1β 28 or clusterin levels tend to have lower Mini-Mental State Examination (MMSE) scores

  • We found that the MMSE scores reflecting cognitive ability were negatively correlated with plasma APL1β 28 and clusterin levels in aMCI patients but not in the levels of healthy controls

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Summary

Introduction

Amnestic mild cognitive impairment (aMCI), which affects 5–6% of people older than 65, is a syndrome attributed to people with noticeable impairments in memory function but whose other cognitive functions are normal[1,2,3,4,5,6,7,8]. The relationship between the plasma concentrations of APL1β 28 and clusterin, two potential biomarkers implicated in APP processing and metabolism, has not been examined in the aMCI population. Body mass index (BMI) has been shown to be associated with the CSF biomarkers of amyloid and tau in MCI patients[83]. Whether these factors, combined with plasma APL1β 28 and clusterin levels, might have a synergic effect remains to be determined. We focused our analysis on aMCI populations and aimed to investigate whether plasma levels of APL1β 28 and clusterin are correlated with cognitive status in the aMCI population and whether these correlations have relationships with other risk factors associated with aMCI and AD

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