Abstract
Alzheimer's disease represents the most common age-related neurodegenerative disorder and a leading cause of progressive cognitive impairment. Predicting cognitive decline is challenging but would be invaluable in an increasingly aging population which also experiences a rising cardiovascular risk. In order to examine whether plasma measurements of one of the established biomarkers of heart failure, brain natriuretic peptide (BNP), reflect a decline in cognitive function, associated with Alzheimer's disease neurodegeneration, BNP levels were analysed, by using a novel assay called a SOMAscan, in 1. cognitively healthy, control subjects; 2. subjects with mild cognitive impairment, and 3. subjects with Alzheimer's disease. The results of our study show that the levels of the BNP were significantly different between the three types of diagnoses (p < 0.05), whereby subjects with mild cognitive impairment had the lowest mean BNP value, and healthy subjects had the highest BNP value. Importantly, our results show that the levels of the BNP are influenced by the presence of at least one APOE4 allele in the healthy (p < 0.05) and in the Alzheimer's disease groups of subjects (p < 0.1). As the levels of the BNP appear to be independent of the APOE4 genotype in subjects with mild cognitive impairment, the results of our study support inclusion of measurements of plasma levels of the BNP in the list of the core Alzheimer's disease biomarkers for identification of the mild cognitive impairment group of patients. In addition, the results of our study warrant further investigations into molecular links between Alzheimer's disease-type cognitive decline and cardiovascular disorders.
Highlights
Impairment in cognitive function or dementia is one of salient features of several age-related neurodegenerative disorders including Alzheimer’s neurodegeneration
In order to determine whether plasma measurements of brain natriuretic peptide (BNP)-32 reflect a decline in cognitive function associated with AD-type neurodegeneration, BNP-32 levels were analysed in subjects that were recruited and examined in seven different European medical centres, according to the criteria described in Data cleaning and preprocessing sub-section of the Materials and methods section
BNP-32 values, as measured by the SOMAscan, were analysed in 634 subjects, grouped according to their diagnoses into 1. control or healthy subjects, 2. subjects who were diagnosed with mild cognitive impairment (MCI) and 3. subjects who were diagnosed with probable AD (Table 1)
Summary
Impairment in cognitive function or dementia is one of salient features of several age-related neurodegenerative disorders including Alzheimer’s neurodegeneration. According to the most recent report published by the Alzheimer’s Disease International organisation, it has been estimated that 46.8 million people worldwide were suffering from dementia in 2015 (World Alzheimer Report 2016: https://www.alz.co.uk/research/world-report-2016). Faced with large number of people suffering from decline in cognitive function worldwide, there is an urgent need for early and accurate detection of cognitive dysfunction. Protein biomarker(s) that could be measured from an accessible biological fluid, such as blood, would be an invaluable tool in serving as a) a diagnostic marker or b) a marker of disease progression, for an incurable neurodegenerative disorder such as Alzheimer’s disease (AD) [1, 2]. Based on the values of BNP and NTproBNP, patients can be stratified into different clinical prognosis stage groups, regardless of their values being obtained for the left ventricular ejection fraction (LVEF) and other hemodynamic parameters (echocardiographic findings related to the left ventricle) [11]
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