PhD Scientific Days 2017

Poster Presentation: Neurosciences

P53: NEUROPROTECTIVE EFFECTS OF THE CYCLOPHILIN D DEFICIENCY IN β-AMYLOID MOUSE MODEL

Előadó neve

Horváth, Gergő

Előadó munkahelye

Department of Medical Biochemistry, MTA-SE Laboratory for Neurochemistry, Semmelweis University

Előadó telefonszáma

+36703343160

Előadó e-mail címe

horvath.gergo@med.semmelweis-univ.hu

Az előadás címe

NEUROPROTECTIVE EFFECTS OF THE CYCLOPHILIN D DEFICIENCY IN β-AMYLOID MOUSE MODEL

Szerző(k) neve és munkahelye

Gergo Horvath1, Mátyás Horváth1, Krisztina Tóth1, Gergely Svab1, Vera Adam-Vizi1, Laszlo Tretter1
1. Department of Medical Biochemistry, MTA-SE Laboratory for Neurochemistry, Semmelweis University

Szekció

Poster Presentation: Neurosciences

Data of the presenter

Doctoral School: János Szentágothai School of Neurosciences
Program: Functional Neurosciences
Supervisor: Tretter László
E-mail address: horvath.gergo@med.semmelweis-univ.hu

Text of the abstract

INTRODUCTION: The accumulation of amyloid β (Aβ) and tau proteins in the brain is the fundamental of Alzheimer disease. In the early phase of the disease the Aβ binds to the mitochondrial proteins and cause bioenergetic failure and increased oxidative stress, which can induce neuronal death. The mitochondrial cyclophylin D (CypD) protein is a major component and regulator of mitochondrial permeability transition pore. In our experiments the gene deletion of CypD (CypD-KO) protein has a neuroprotective effect in the present of Aβ.
AIM: Our goal was to cross transgenic mice overexpressing a mutant human form of amyloid precursor protein and mutated presenilin1 with CypD-KO. In our experiments mitochondrial functions were examined.
METHODS: Our experiments were done on isolated brain mitochondria from 4 different mice (wild-type, Alzheimer’s mouse model (Alz), CypD-KO and crossed Alz/CypD). The mitochondrial respiration was measured by Clark-type electrode. The mitochondrial H2O2 production with Amplex UltraRed fluorimetry. The ATP production was measured a with linked spectrophotometric assay.
RESULTS: During our measurements the Alz mice showed decreased O2 consumption, ATP production and elevated H2O2 production versus the wild type control. The bioenergetic parameters of Alz/CypD samples were improved compared to Alz. The Alz/CypD results were comparable to CypD.
CONCLUSIONS: From our investigations of Alzheimer’s mouse model we was led to conclude that mitochondria functions were impaired, but knocking out the CypD protein improved bioenergetic parameters. Our results showed that inhibitiors of CypD protein can be potential drug candidates in neurodegenerative diseases.

Fundings OTKA (NK 81983), MTA (MTA TKI 2013), Hungarian Brain Research Program (KTIA_13_NAP-A-III/6) to V.A-V.

Azonosító

P53

Kind

Szabad

Előadás fájl jóváhagyás

nem rendelkezett róla

Előadó

1239

Authors (legacy)

Gergo Horvath1, Mátyás Horváth1, Krisztina Tóth1, Gergely Svab1, Vera Adam-Vizi1, Laszlo Tretter1
1. Department of Medical Biochemistry, MTA-SE Laboratory for Neurochemistry, Semmelweis University