Claudia Cicognola, Sweden

Lund University Clinical Memory Research Unit
In 2014, I obtained my MD at the University of Perugia, Italy. Here, I worked at the Memory Clinic led by Professor Lucilla Parnetti. My research focus was on diagnostic accuracy of cerebrospinal fluid (CSF) biomarkers in memory impairment and dementia due to Alzheimer’s disease (AD). In 2019, I completed my PhD in Kaj Blennow’s lab at the University of Gothenburg, Sweden. Here I studied tau protein and its role in the pathogenesis and as a biomarker of AD and tauopathies. During the PhD, I developed immunoassays targeting several different tau species in CSF and brain extracts. The assays were applied successfully to independent clinical cohorts. My work resulted in publications in high impact journals on their role as biomarkers in AD and tauopathies and their relationship with tau-PET data. Since 2020, I work both clinically at the Memory Clinic at Skåne University Hospital, Malmö, and as a postdoctoral researcher in Oskar Hansson’s lab at the Clinical Memory Research Unit, Lund University. My focus is on blood biomarkers for AD within the Swedish BioFINDER study. In 2020, I received the Bundy Academy Award for Neurology.

Presenter of 2 Presentations

PLASMA GLIAL FIBRILLARY ACIDIC PROTEIN PREDICTS AMYLOID STATUS AND FUTURE CONVERSION TO ALZHEIMER’S DISEASE IN A MILD COGNITIVE IMPAIRMENT LONGITUDINAL COHORT

Session Type
SYMPOSIUM
Date
12.03.2021, Friday
Session Time
12:00 - 14:00
Room
On Demand Symposia D
Lecture Time
12:30 - 12:45
Session Icon
On-Demand

Abstract

Aims

Astrogliosis in response to amyloid-beta (Aβ) plaques is an early feature of Alzheimer's disease (AD). Glial fibrillary acidic protein (GFAP) is expressed in astrocytes and is increased in CSF in AD. Studies on plasma GFAP as AD biomarker are few and not longitudinal. Our aim was to evaluate plasma GFAP as potential biomarker for Aβ status and for future development of AD dementia.

Methods

161 subjects with a baseline clinical diagnosis of mild cognitive impairment (MCI) were included, genotyped for APOE, followed for 4.7 years (average) and assessed for conversion to AD at follow-up. Plasma was collected at baseline and follow-up. GFAP was measured with Simoa GFAP Discovery kit for SR-X (Quanterix). Aß positivity (Aß+) was defined as CSF Aβ42/40 <0.07 (cut-off calculated with Youden index within the cohort).

Results

Baseline GFAP was increased in Aβ+ MCI patients (p<0.0001). Plasma GFAP could predict Aβ+ status (p<0.0001, AIC=184.3, AUC=0.787, sensitivity=73%, specificity=75%). Accuracy was increased by combining plasma GFAP and APOE genotype (p<0.0001, AIC 154.7, AUC=0.859). Plasma GFAP could also predict subsequent development of AD dementia (p<0.0001, AIC=154.4, AUC=0.836, sensitivity=72%, specificity=85%). Predictive accuracy of future AD dementia was improved by combining plasma GFAP with APOE genotype and age (p<0.0001, AIC=140, AUC=0.864). Longitudinal slopes showed a significant increase of plasma GFAP over time in Aβ+ MCI compared to Aβ- (p<0.0001) and in subjects later diagnosed with AD compared to those that remained clinically stable (stable Aβ-:p<0.0001; stable Aβ+:p=0.049).

Conclusions

Plasma GFAP is strongly associated to Aβ status and is a good predictor of clinical evolution to AD.

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