Abstract
Peripheral inflammation mechanisms involved in Alzheimer's disease (AD) have yet to be accurately characterized and the identification of blood biomarker profiles could help predict cognitive decline and optimize patient care. Blood biomarkers described to date have failed to provide a consensus signature, which is mainly due to the heterogeneity of the methods used or the cohort. The present work aims to describe the potential informativity of peripheral inflammation in AD, focusing in particular on the potential association between the level of plasma neurofilament light (NFL), peripheral inflammation (by quantifying IL-1β, IL-6, TNFα, CCL5, TNF-R1, sIL-6R, TIMP-1, IL-8 in blood) and cognitive decline (assessed by the MMSE and ADAScog scales) through a 2-year follow-up of 40 AD patients from the Cytocogma cohort (CHU Poitiers, Pr M. Paccalin). Our results show for the first time a strong correlation between plasma NFL and TNF-R1 at each time of follow-up (baseline, 12 and 24 months), thus opening an interesting perspective for the prognosis of AD patients.
Highlights
Alzheimer’s disease (AD) is a neurodegenerative pathology characterized by progressive cognitive impairment, leading to a loss of autonomy
We evaluated the potential informativity of peripheral inflammation in AD: our study aims to describe the potential association between plasma neurofilament light (NFL) level, peripheral inflammation and cognitive decline, through a 2-year follow-up of 40 AD patients from the Cytocogma cohort
We examined the level of expression of plasma biomarkers of inflammation (TNFa and its receptor [TNF-R1], IL-6 and its receptor [sIL-6R], CCL5, IL-8, IL-1b, TIMP-1) and NFL, in 40 AD patients of Cytocogma cohort[32], half of whom were considered to be slow decliner and half fast decliners
Summary
Alzheimer’s disease (AD) is a neurodegenerative pathology characterized by progressive cognitive impairment, leading to a loss of autonomy. The role of tumor necrosis factor-alpha (TNFa) in brain neuropathology is widely described, with the pro-inflammatory cytokine being increased in plasma and cerebrospinal fluid (CSF) in AD p atients[7]. Soluble Aβ peptides can trigger microglial activation in vitro and in vivo, resulting in the subsequent release of pro-inflammatory actors, such as IL-1b This chemokine is described as elevated in CSF and brain tissue in AD p atients[19], while serum levels remain stable[8] or elevated[20] in AD patients compared to control, depending on the studies. TIMP-1 (the tissue inhibitor of MMP9) is significantly lower in plasma of AD patients than in c ontrols[23], while it increases in the CSF of patients with AD and Mild Cognitive Impairment (MCI)[8,24]. Discrepancies are described concerning IL-6 and its receptor (sIL-6R), with studies describing decrease of plasmatic IL-68,21 and sIL-6R8 in AD patients (compared to control), and others describing a stability of this cytokine in the same context[20]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
