PhD Scientific Days 2023

Neurosciences II.

Microglial Involvement in Alzheimer’s Disease and the Possible Role of SORL1

Előadó neve

Dr. Pósfai, Balázs, PhD

Neptun code

AE4W0Q

Előadó munkahelye

Institute of Experimental Medicine

Előadó telefonszáma

06303313010

Előadó e-mail címe

bposfai91@gmail.com

Az előadás címe

Microglial Involvement in Alzheimer’s Disease and the Possible Role of SORL1

Szerző(k) neve és munkahelye

Balázs Pósfai1, Nikolett Lénárt1, Krisztina Tóth1, Anna Kellermayer1, Sára Vida1, Dóra Anett Schwarcz1, Zsolt Lele2, Csaba Cserép1, Ádám Dénes1
Laboratory of Neuroimmunology, Institute of Experimental Medicine, Budapest
Laboratory of Molecular Neurobiology, Institute of Experimental Medicine, Budapest

Bemutatás módja

Szóbeli

Szekció

Neurosciences II.

Language of the presentation

English

Preferred session

Neurosciences

Összefoglaló szövege

Introduction: Understanding the mechanisms of neurological diseases is one of the most urgent challenges of medicine. In recent years, our workgroup has contributed to the understanding of the homeostatic and neuroprotective roles of microglia, the brain’s main immune cell under both physiological and pathological conditions. Alzheimer’s disease (AD) is a progressive neurodegenerative disease that is the leading cause of dementia worldwide. In our ongoing experiments, we are exploring the involvement of microglia in the pathogenesis of AD, specifically focusing on microglia-neuron somatic junctions, and on the role of the sortilin receptor SORL1, the genetic alteration of which shows a strong correlation with hereditary late-onset AD.
Aims: To assess microglial alterations during the pathogenesis of AD, and study the role of AD-related risk protein SORL1.
Methods: In order to conduct a translational study, we utilize both mouse and human samples. We have collected fixed tissue, native brains and cerebrospinal fluid of triple-transgenic AD-model (PSEN1//App_swe//tauP301L) and control mice, from three different age groups (60-80 days, 220-240 days, 490-520 days) and both sexes. We have also developed a new plasmid and performed in utero electroporation, resulting in the deletion of SORL1 protein in a subpopulation of cortical neurons in transgenic mice. We are processing these samples primarily for cytokine measurements and high-resolution immunofluorescent imaging. We also obtained 3 groups of human CSF samples: SORL1-mutation carrying AD patients, age-matched non-SORL1-related AD and CTRL patients.
Results and conclusions: Our preliminary results show significant alterations of microglia during the aging of AD-model mice, as well as a different dynamic to the expression changes of SORL1-protein. The evaluation of microglia-neuron contacts and cytokine expression levels in both the mouse and the human samples is ongoing.
Funding: Supported by SORLA-FIX JPND and by the ÚNKP-22-4-I-SE-7 New National Excellence Program of the Ministry for Innovation and Technology from the source of the National Research, Development and Innovation Fund.

University and Doctoral School

Semmelweis University, János Szentágothai Doctoral School of Neurosciences

Supervisor

Ádám Dénes, Csaba Cserép

Publication of my abstract

I do not give consent to the publication of my abstract on the website of the congress.

Kind

Szabad

Status

elfogadva

Accepted presentation method

szóbeli

Előadás fájl jóváhagyás

nem rendelkezett róla

Előadó

4093

Start

15:30

End

15:45

Authors (legacy)

Balázs Pósfai1, Nikolett Lénárt1, Krisztina Tóth1, Anna Kellermayer1, Sára Vida1, Dóra Anett Schwarcz1, Zsolt Lele2, Csaba Cserép1, Ádám Dénes1
Laboratory of Neuroimmunology, Institute of Experimental Medicine, Budapest
Laboratory of Molecular Neurobiology, Institute of Experimental Medicine, Budapest