Poster preview
ePoster
CHARACTERIZATION OF NOGO-A–MEDIATED MECHANISMS UNDERLYING DOPAMINERGIC AND MITOCHONDRIAL DYSREGULATION IN AN IPSC-DERIVED PARKINSON’S DISEASE MODEL
Sara Alonso Jiménezand 3 co-authors
University of Bern
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS04-08PM-148
Presentation
Date TBA
Board: PS04-08PM-148
Event Information
Poster Board
PS04-08PM-148
Poster
View posterAbstract
Nogo-A, a myelin-associated protein, was demonstrated to inhibit axonal regeneration, thus limiting the ability for repair within the central nervous system. Its involvement in synaptic regulation, myelin maintenance, and mitochondrial homeostasis has raised interest in its role in Parkinson’s disease (PD). In particular, understanding Nogo-A’s multifaceted role in the involvement of dopaminergic neuronal survival may provide insights into PD pathophysiology and potential therapeutic targets.
We examined the effects of Nogo-A on neuronal development and neurodegeneration using wild-type (WT) and Nogo-A knockout (KO) human induced pluripotent stem cell (hiPSC)-derived dopaminergic neurons. To model PD-related stress, cells were exposed to 6-hydroxydopamine (6-OHDA). Viability, oxidative stress, mitochondrial function, and electrophysiology were assessed using proteomics, qPCR, functional assays, and high-density multi-electrode array (HD-MEA).
6-OHDA treatment reduced cell viability and increased oxidative stress across both genotypes. Nogo-A KO cultures exhibited a higher basal proportion of tyrosine hydroxylase (TH)-positive cells, suggesting enhanced dopaminergic differentiation. Nogo-A-KO neurons displayed a significant upregulation of dopaminergic markers, including TH and LMX1A, although survival rates following 6-OHDA were comparable between genotypes. Preliminary results show that Nogo-A-KO neurons exhibited higher baseline superoxide levels; however, their functional mitochondria parameters diverged from those of WT neurons under stress conditions.
These findings suggest that Nogo-A influences dopaminergic homeostasis and mitochondrial dynamics. The observed differences in KO cells highlight the complex role of Nogo-A and warrant further investigation regarding the underlying molecular pathways for stress response modulation.
We examined the effects of Nogo-A on neuronal development and neurodegeneration using wild-type (WT) and Nogo-A knockout (KO) human induced pluripotent stem cell (hiPSC)-derived dopaminergic neurons. To model PD-related stress, cells were exposed to 6-hydroxydopamine (6-OHDA). Viability, oxidative stress, mitochondrial function, and electrophysiology were assessed using proteomics, qPCR, functional assays, and high-density multi-electrode array (HD-MEA).
6-OHDA treatment reduced cell viability and increased oxidative stress across both genotypes. Nogo-A KO cultures exhibited a higher basal proportion of tyrosine hydroxylase (TH)-positive cells, suggesting enhanced dopaminergic differentiation. Nogo-A-KO neurons displayed a significant upregulation of dopaminergic markers, including TH and LMX1A, although survival rates following 6-OHDA were comparable between genotypes. Preliminary results show that Nogo-A-KO neurons exhibited higher baseline superoxide levels; however, their functional mitochondria parameters diverged from those of WT neurons under stress conditions.
These findings suggest that Nogo-A influences dopaminergic homeostasis and mitochondrial dynamics. The observed differences in KO cells highlight the complex role of Nogo-A and warrant further investigation regarding the underlying molecular pathways for stress response modulation.
Recommended posters
HUMAN MIDBRAIN ORGANOIDS REVEAL THE CHARACTERISTICS OF AXONAL MITOCHONDRIA SPECIFIC TO DOPAMINERGIC NEURONS
Masato Koike, Akihiko Nishijima, Soichiro Kakuta, Akihiro Yamaguchi, Kei-ichi Ishikawa, Hideyuki Okano, Wado Akamatsu, Nobutaka Hattori, Mutsumi Yokota
MODELING GENETIC HETEROGENEITY IN PARKINSON’S DISEASE USING PATIENT-DERIVED DOPAMINERGIC NEURONS AND MULTI-OMICS APPROACHES
Federica Carrillo, Giorgio Fortunato, Arianna Coppola, Marco Ghirimoldi, Nwife Getrude Okechukwu, Vittoria Federica Borrini, Shahzaib Khoso, Antonietta Di Lorenzo, Mariarca Marciano, Giuseppe Giurin, Francesca D’amato, Cristina D’Aniello, Alessandro Fiorenzano, Teresa Nutile, Danilo Licastro, Sara Pietracupa, Nicola Modugno, Katiuscia Martinello, Sergio Fucile, Marcello Manfredi, Annalisa Fico, Teresa Esposito
RESTORATION OF NADH OXIDATION IN DOPAMINERGIC NEURONS PREVENTS PARKINSONISM
Esther García Benítez, Karis B D’Alessandro, Alejandro Jiménez-Medina, Enrico Zampese, Xavier d’Anglemont de Tassigny, Claudia García-Rodríguez, James Surmeier, José López-Barneo, Patricia González-Rodríguez
MODULATION OF NEUROTROPHIC SIGNALING PATHWAYS IN NEURONAL DYSFUNCTION ASSOCIATED WITH PARKINSON’S DISEASE
Daniele Pensabene, Noemi Martella, Michela Varone, Emanuele Bisesto, Mayra Colardo, Sandra Moreno, Marco Segatto
NEURON-SPECIFIC METABOLIC DYSFUNCTION TRIGGERS SYSTEMIC REMODELING IN A PARKINSONIAN MOUSE MODEL
Claudia García-Rodríguez, Alejandro Jiménez-Medina, Esther García-Benitez, José López-Barneo, Xavier d’Anglemont de Tassigny, Patricia González-Rodríguez
DISSECTING MICROGLIA-ASTROCYTE CROSSTALK AND CCL2-MEDIATED NEURONAL VULNERABILITY IN PARKINSON’S DISEASE USING IPSC-DERIVED MODELS
Jara Montero Muñoz, Veronica Testa, Valentina Baruffi, Styliani Stavroulaki, Marta Puppo, Eshani Chandnani, Loris Mularoni, Yvonne Richaud, Christin Weissleder, Michela Deleidi, Stefano Pluchino, Angel Raya, Antonella Consiglio