Intern
    Institut für Anatomie und Zellbiologie

    Neurodegeneration

    Team:

    Prof. Dr. I. Dudanova irina.dudanova@uni-wuerzburg.de

    Neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease and Huntington’s disease are age-dependent, so far incurable disorders that are becoming increasingly prevalent in our aging society. At the cellular level, these diseases are characterized by progressive dysfunction and ultimate loss of neurons. Another common hallmark of neurodegenerative disorders is misfolding and aggregation of certain proteins such as Aβ, Tau, α-synuclein or mutant Huntingtin. However, it is still unclear why certain populations of neurons are particularly vulnerable to degeneration, while other neurons in their vicinity remain largely intact. Moreover, we lack understanding of how the demise of the vulnerable neuronal cell types affects the functionality of neural circuits, and how these changes are linked to behavioral defects.

    To address these questions, we investigate the effects of protein aggregates on the cellular functions as well as on the activity of neuronal networks (Hosp et al., 2017; Burgold et al., 2019; Blumenstock and Dudanova, 2020; Blumenstock et al., 2021; Riera-Tur et al., 2022; Voelkl et al., 2022; Blumenstock et al., 2025; Feigenbutz et al., 2025).Based on these findings, our goal is to identify molecular pathways and neural circuit impairments that play a role in neuronal vulnerability and could provide promising targets for new therapeutic approaches (Voelkl et al., 2023; Blumenstock et al., 2025; Da Silva Padilha et al., 2025).
    We work with a range of model systems including cell culture and genetic mouse models, using a combination of molecular and histological approaches, behavioral analyses and in vivo imaging.

    The major current directions of our research are:

    1. Determining the role of protein quality control in neurodegeneration
    2. Deciphering cortical circuit alterations in neurodegenerative diseases
    3. Designing disease-modifying strategies

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    Publications:

    2025

    2023

    2022

    2021

    2020

    2019

    2017

    2015

    • Born G, Grayton HM, Langhorst H, Dudanova I, Rohlmann A, Woodward BW, Collier DA, Fernandes C, Missler M.
      Genetic targeting of NRXN2 in mice unveils role in excitatory cortical synapse function and social behaviors.
      Front Synaptic Neurosci. 2015 Feb 19;7:3. doi: 10.3389/fnsyn.2015.00003. PMID: 25745399; PMCID: PMC4333794.
       
    • Gaitanos T*, Dudanova I*, Sakkou M, Klein R, Paixao S* (2015) The Eph Receptor Family (Book chapter) in Receptor Tyrosine Kinases: Family and Subfamilies, Edited by Deric L. Wheeler and Yosef Yarden (Springer International Publishing Switzerland), 165-264; doi: 10.1007/978-3-319-11888-8_5 -  *equal contribution

    2014

    2013

    2012

    2011

    2010

    2008

    2007

    • Dudanova I, Tabuchi K, Rohlmann A, Südhof T, Missler M (2007) Deletion of a-neurexins does not cause a major impairment of axonal pathfinding or synapse formation. J Comp Neurol 502(2): 261-274. PMID: 17347997

    2006

    • Dudanova I*, Sedej S*, Ahmad M*, Masius H, Sargsyan V, Zhang W, Riedel D, Angenstein F, Schild D, Rupnik M, Missler M (2006) Important contribution of a-neurexins to Ca2+-triggered exocytosis of secretory granules. J Neurosci 26(41):10599-10613. PMID: 17035546 - *equal contribution
       
    • Piechotta K, Dudanova I, Missler M (2006) The resilient synapse: insights from genetic interference of synaptic cell adhesion molecules (Review). Cell Tissue Res 326(2):617-42. PMID: 16855838