Somatostatin and Neuropeptide Y in Cerebrospinal Fluid: Correlations With Amyloid Peptides Aβ1–42 and Tau Proteins in Elderly Patients With Mild Cognitive Impairment

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.

Somatostatin, Olfaction, and Neurodegeneration

“…Remarkably, SST is the main binder of Aβ 1−42 and can encourage the formation of different Aβ 1−42 oligomers by acquiring amyloid properties (Wang et al, 2017;Solarski et al, 2018). In agreement with this, SST and Aβ 1−42 levels in the cerebrospinal fluid seem to be correlated (Duron et al, 2018) and co-localization of both in the human brain, including the olfactory cortex, are widespread histological features . In fact, SST has been highlighted as a regulator of Aβ 1−42 deposition (Saito et al, 2005).…”

Identification of KIAA0513 and Other Hub Genes Associated With Alzheimer Disease Using Weighted Gene Coexpression Network Analysis

“…According to GO and KEGG analyses, the DEGs identified by combined analysis were mostly enriched in synapse function, and genes from the key module were mostly related to learning and memory, which are closely correlated with AD onset. Among these DEGs, we identified some robust genes that played vital roles in AD pathogenesis, such as SERPINA3 ( Kamboh et al, 2006 ), CD163 ( Pey et al, 2014 ), and SST ( Duron et al, 2018 ; Solarski et al, 2018 ).…”

Enhanced neprilysin-mediated degradation of hippocampal Aβ42 with a somatostatin peptide that enters the brain

“…Among these, the subtypes SSTR1 and SSTR4 are highly expressed in the hippocampus and neocortex 32 , 33 . The levels of SST decrease in the brain and cerebrospinal fluid (CSF) with age and in patients with AD, potentially as an effect of the loss of somatostatinergic interneurons 34 , 35 . This decline is considered to be one of the earliest biochemical changes in the AD brain, which also include abnormalities in the SSTR expression and density 36 .…”