Pieter Jelle Visser (Netherlands)
Amsterdam University Medical Center and Maastricht University
Alzheimer center
Pieter Jelle Visser, MD, PhD, is a clinical epidemiologist at Maastricht University and Amsterdam University Medical Center in the Netherlands and is visiting professor at the Karolinska Institute in Stockholm, Sweden. His research focuses on the pathophysiology, diagnosis, prognosis and treatment of predementia Alzheimer’s disease by combining different modalities such as imaging, proteomics, genetics and digital markers. He also coordinates projects that enable datasharing and data pooling in the AD field such as the Netherlands Consortium of Dementia Cohorts (NCDC), the Amyloid Biomarker Study (ABS), and the European Platform forNeurodegenerative Disorders (EPND).

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 Conference Calendar

PROTEOMIC CORRELATES OF AMYLOID BETA AND TAU IN CSF. A MONOZYGOTIC TWIN STUDY

Session Name
1340 - AD, PD, MSA MECHANISMS, DIAGNOSIS, BIOMARKERS, IMAGING & TRASLATIONAL DRUG DEVELOPMENT (ID 233)
Session Type
SYMPOSIUM
Date
Fri, 18.03.2022
Session Time
05:15 PM - 07:15 PM
Room
ONSITE: 133-134
Lecture Time
06:30 PM - 06:45 PM
Presenter

Abstract

Aims

Early Alzheimer’s disease (AD) is characterised in cerebrospinal fluid (CSF) by a decreased concentration of amyloid beta 1-42 and and an increase in tau. Aim of this study was to identify processes associated with abeta and tau pathology in cognitively normal monozygotic twins.

Methods

We included 126 twins (54 pairs) from the PreclinAD study. We assessed 690 proteins by OLINK multiplex panels and total-tau (t-tau), abeta42, abeta40 by ELISA. The abeta42/40 ratio was used as measure of amyloid pathology. We correlated the abeta42/40 ratio and t-tau levels with all proteins. For proteins that showed an association with abeta42/40 or t-tau we performed Cross-Twin Cross-Trait (CTCT) analysis by correlating the concentration of abeta42/40 or t-tau in one twin with the concentration of a protein in the co-twin. Enrichment analysis was performed using Gene Ontology.

Results

Average age was 70 years. The Abeta42/40 ratio correlated positively with 3 proteins of which one correlated with abeta42/40 in CTCT analysis. The abeta 42/40 ratio correlated negatively with 114 proteins, which were enriched for apoptosis (p=7.8*10-11) and cytokine production (p=3.7*10-9). Three proteins correlated with abeta42/40 in CTCT analysis. T-tau correlated positively with 414 proteins which were enriched for nervous system development (p=9.7*10-21). 335 of these proteins correlated with t-tau in CTCT analysis. T-tau correlated negatively with 21 proteins which were enriched for leukocyte migration (p=9.7*10-3). Seven proteins correlated with t-tau in CTCT analysis.

Conclusions

Increased amyloid pathology was associated apoptosis and cytokine production. Increases in t-tau were associated with neuronal plasticity and these associations had a shared genetic background.

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