Yanaika S. Hok-A-Hin (Netherlands)
Amsterdam UMC
Clinical Chemistry
Yanaika Hok-A-Hin is a PhD student at the Neurochemistry Laboratory, Amsterdam University Medical Center. She has gained expertise in developing immuno-based assay on state of the art technologies, such as ultrasensitive and array-based technologies. Her research project focuses on the further validation of novel cerebrospinal fluid biomarkers for Alzheimer’s Disease identified by proteomics discovery studies. She aims to develop a panel of CSF biomarkers that reflect the complex biology of Alzheimer’s Disease that could aid in the discrimination of Alzheimer’s Disease from other types of dementias.

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APOLIPOPROTEIN L1 IS INCREASED IN FRONTOTEMPORAL LOBAR DEGENERATION POST-MORTEM BRAIN TISSUE BUT NOT IN CEREBROSPINAL FLUID

Session Name
0410 - TDP43- AND C9ORF72-RELATED DISEASES 1 (ID 60)
Session Type
SYMPOSIUM
Date
Wed, 16.03.2022
Session Time
04:15 PM - 06:15 PM
Room
ONSITE: 133-134
Lecture Time
04:45 PM - 05:00 PM
Presenter

Abstract

Aims

Frontotemporal dementia (FTD) is caused by frontotemporal lobar degeneration (FTLD), characterized by inclusions of tau (FTLD-Tau) or TDP43 (FTLD-TDP). Cerebrospinal fluid (CSF) biomarkers are needed for the diagnosis of FTD and its pathological subtypes. Our CSF proteomics study showed increased Apolipoprotein L1 (APOL1), involved in lipid metabolism, in FTD with stronger levels in FTLD-Tau. Here, we aimed to characterize APOL1 in FTLD post-mortem brain tissue with definite pathology and validate its potential as a FTD biomarker.

Methods

APOL1 levels were analyzed in frontal cortex of FTLD (n=62, including 23 FTLD-Tau and 29 FTLD-TDP) and non-demented controls (n=18) either by immunohistochemistry, western blot or our in-house ELISA. The association of APOL1 immunoreactivity with phosphorylated Tau (pTau) and TDP-43 (pTDP43) was assessed. CSF APOL1 was measured in FTD patients (n=27, including 12 FTLD-Tau and 15 FTLD-TDP) and controls (n=15) by ELISA

Results

APOL1 levels were significantly increased in the frontal cortex of FTLD cases using three different technologies. No differences between FTLD pathological subtypes were detected. APOL1 immunoreactivity was observed in neuronal and glia cells. No association with the main FTLD proteinopathies (pTau or pTDP43) was detected. In CSF, the levels of APOL1 were comparable between FTD patients and controls, and between FTLD pathological subtypes.

Conclusions

We show increases of APOL1 in FTLD pathology irrespective of the subtypes. APOL1 changes were not detected in CSF using the current immunoassay, therefore, novel assays need to be developed. Future research should also explore the specific role APOL1 plays within FTLD pathogenesis.

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