Abstract
A combination of low cerebrospinal fluid (CSF) Amyloid β1–42 (Aβ1–42) and high Total-Tau (T-Tau) and Phosphorylated-Tau (P-Tau) occurs at a prodromal stage of Alzheimer’s disease (AD) and recent findings suggest that network abnormalities and interneurons dysfunction contribute to cognitive deficits. Somatostatin (SOM) and Neuropeptide Y (NPY) are two neuropeptides which are expressed in GABAergic interneurons with different fates in AD the former only being markedly affected. The aim of this study was to analyze CSF SOM, NPY and CSF Aβ1–42; T-Tau, P-Tau relationships in 43 elderly mild cognitively impairment (MCI) participants from the Biomarker of AmyLoïd pepTide and AlZheimer’s disease Risk (BALTAZAR) cohort. In these samples, CSF SOM and CSF Aβ1–42 on the one hand, and CSF NPY and CSF T-Tau and P-Tau on the other hand are positively correlated. CSF SOM and NPY concentrations should be further investigated to determine if they can stand for early AD biomarkers.Clinical Trial Registration: www.ClinicalTrials.gov, identifier #NCT01315639.
Highlights
Alzheimer’s disease (AD) neuropathology is characterized by intraneuronal protein clusters of hyperphosphorylated Tau protein and extracellular amyloid beta (Aβ) protein aggregation that start decades before the occurrence of clinical symptoms (Bateman et al, 2012; Epelbaum et al, 2017)
The present results indicate that high cerebrospinal fluid (CSF) SOM and high CSF Amyloid β1–42 (Aβ1–42) concentrations on the one hand and high CSF Neuropeptide Y (NPY) and high CSF Tau and P-Tau concentrations on the other hand, are correlated in a small population of elderly subjects suffering from mild cognitively impairment (MCI)
High CSF NPY concentrations are related to male gender, diabetes, and low plasma cholesterol
Summary
Alzheimer’s disease (AD) neuropathology is characterized by intraneuronal protein clusters of hyperphosphorylated Tau protein (neurofibrillary tangles) and extracellular amyloid beta (Aβ) protein aggregation that start decades before the occurrence of clinical symptoms (Bateman et al, 2012; Epelbaum et al, 2017). The combination of low Aβ1–42 and high T-Tau or p-Tau, which occurs at a prodromal stage of AD (Hansson et al, 2006) and even before clinical impairment (Sutphen et al, 2015) has a sensitivity of 90%–95% and a specificity of about 90% in AD diagnosis (de Souza et al, 2011; Gabelle et al, 2013; Lehmann et al, 2014). In this way, an individual patient’s risk estimation of any-type dementia can be improved by adding CSF biomarker information to clinical and imaging tests as recommended in routine care (Handels et al, 2017; Albert et al, 2018). A low level of CSF SOM correlates with cognitive deficits in AD (Tamminga et al, 1987) while CSF NPY concentrations changes are not as well documented (Gabriel et al, 1993)
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