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24.04.2026, Friday, 11:30-13:00
The brain is the most complicated and vulnerable organ in the body. Physical injuries, environmental changes, pollution, and genetic mutations can result in severe dysfunctions that present with nonspecific symptoms and are difficult to classify. The limited and challenging nature of human brain research encourage to investigate various animal models. The session will be divided into two parts: the use of an alternative model, Drosophila melanogaster and mammalian models. Invited speaker Alex Whithworth is an expert in Parkinson’s disease research. He will introduce the audience to how to use Drosophila as a model, and he will present his data about the role of mitophagy in PD. The next two early-stage researcher speakers will follow the same model. Justyna Kadłuczka will show the data about the effect of synuclein expression in the photoreceptor cells on the retina and brain functioning. Zuzanna Kula will present the data about the possibility of using inhibitors of glusylceramidase beta in PD treatment. The next part will be focused on mammalian models. The first speaker, Aleksandra Klachacz, will show her data about the role of astrocytic factors in the post-ischemic brain. To cover a variety of models, this talk will be followed by Chin Long Poo who will present how optimized rotenone exposure accelerated dopaminergic dysfunction and Parkinsonian behaviour in adult zebrafish.
MRC Mitochondrial Biology Unit, University of Cambridge, UK
"What can we learn about Parkinson’s disease from fruit flies."
Parkinson’s disease (PD) is a common neurodegenerative movement disorder that is typically caused by a combination of genetic and environmental factors. Relatively rare inherited forms of PD have delivered incredible insights into the pathogenic mechanism and have consistently highlighted defects in proteostasis and mitochondrial dysfunction. Two genes linked to inherited PD, PINK1 and PRKN, provide the strongest links to mitochondrial dysfunction as their encoded proteins (the kinase PINK1 and ubiquitin ligase Parkin) function to signal the selective degradation of mitochondria – a process termed mitophagy. Many aspects of PINK1/Parkin function are deeply conserved through evolution. Since their development, the Drosophila models of the orthologous genes, Pink1 and parkin, have delivered fundamental insights into their physiological function. The strength of the model is due largely to the robust phenotypes of the genetic knockouts, which confer mitochondrial disruption, locomotor deficits, and neurodegeneration under basal conditions. Applying the powerful genetic tools available in Drosophila has uncovered important molecular and cellular aspects of Pink1/parkin disruption to tissue and organismal health. A key advantage of analysing Pink1/parkin function in an animal model is the ability to interrogate inter-organ, such as the gut-brain axis, as well as systemic impacts on neurodegeneration and healthspan. Here, the latest advances of Dr. Alex Whitworth team on understanding the physiological roles of Pink1/parkin as well as the consequences of their dysfunction and therapeutic opportunities.
Institute of Zoology and Biomedical Research, Department of Biology and Cell Imaging, 9 Gronostajowa St., Kraków, Poland
"The link between circadian clock and Parkinson's disease development - research on Drosophila melanogaster model"
Parkinson's disease (PD) is characterized by a progressive loss of dopaminergic neurons within the substantia nigra pars compacta. Although PD is primarily described as a motor disorder, prodromal symptoms such as circadian clock desynchronization, sleep disturbances, and blurred vision may occur years before diagnosis. It has been implicated that non-motor symptoms, especially circadian clock disruption, can exacerbate the progression of PD.
We investigated how mitophagy disruption or the expression of human α-synuclein exclusively in photoreceptors affected retinal function and whether the observed changes might contribute to the development and progression of PD.
In our study, we used a genetic model of PD in Drosophila melanogaster either by silencing park gene or expressing human α-synuclein in the visual system. We performed behavioral analysis: climbing assay, sleep and locomotor activity. We analyzed the external structure of the Drosophila ommatidia using scanning electron microscopy and examined the morphology of the photoreceptors with histological staining. Finally, to determine the number of dopaminergic neurons we immunostained for tyrosine hydroxylase.
We observed that mitophagy disruption reduced the flies’ overall fitness and affected both daytime and nighttime sleep. Synucleinopathy not only altered sleep pattern but also severely disrupted photoreceptor morphology and reduced the number of dopaminergic neurons.
Our data revealed that inducing PD in the visual system affected processes that, in Drosophila, are regulated by distinct central brain structures.
De Montfort University, School of Pharmacy, The Gateway, Leicester, LE1 9BH, United Kingdom
"GBA2 inhibitors as a new approach to treating neurodegenerative diseases"
Toxicology & Pharmacology Unit, Herbal Medicine Research Centre, Institute for Medical Research, National Institutes of Health, Jalan Setia Murni U13/52, 40170 Shah Alam, Selangor, Malaysia; Institute of Planetary Survival for Sustainable Well-being, International Islamic University Malaysia, 25200 Kuantan, Pahang, Malaysia
"Accelerated dopaminergic dysfunction and Parkinsonian behaviour in adult zebrafish following optimized rotenone exposure"
Parkinson’s disease (PD) is the second most common neurodegenerative disease, characterized by the progressive loss of dopaminergic neurons in the substantia nigra and motor impairment. PD can be induced in vivo using specific neurotoxic chemicals. While rotenone is widely used to induce PD-like phenotypes in adult zebrafish, commonly reported protocols employ lower concentrations over prolonged exposure periods, resulting in variability in disease onset and experimental timelines.
This study aims to establish a faster and more consistent rotenone-induced PD model in adult zebrafish using an optimized exposure concentration.
Adult zebrafish were exposed to rotenone at 5 µg/L and 7.5 µg/L for a total of 4 weeks. Locomotor and anxiety-related behaviours were assessed longitudinally from Day 3 to Day 28. Dopamine levels were measured on the last day of assessment.
Zebrafish exposed to 5 µg/L rotenone exhibited Parkinsonian-like motor deficits by Day 19, whereas exposure to 7.5 µg/L induced significant and consistent reductions in total distance travelled and mean swimming speed as early as Day 12. In addition, increased bottom-dwelling behaviour and freezing duration were observed earlier and more robustly in the 7.5 µg/L group, indicating accelerated development of PD-like behavioural phenotypes. Dopamine analysis performed at the late stage of exposure further confirmed dopaminergic impairment in rotenone-treated fish, supporting the observed behavioural deficits. The 7.5 µg/L exposure paradigm produced a stable and reproducible PD-like phenotype within a shorter timeframe compared with the widely established 5 µg/L long-term exposure model.
In conclusion, chronic exposure to rotenone at 7.5 µg/L represents a faster and reliable method for inducing Parkinson’s disease-like phenotypes in adult zebrafish, offering a practical and efficient platform for mechanistic studies and neuroprotective drug screening.
Cellular Neurobiology Research Group, Institute of Developmental Biology and Biomedical Sciences, Faculty of Biology, University of Warsaw
"Astrocyte-secreted factors as key players in the post-ischemic brain"
Ischemic stroke is a major cause of death and long-term disability, affecting millions worldwide, with a significant proportion of people experiencing persistent motor deficits. Astrocytes are key regulators of the brain environment and become activated in response to ischemic injury. Upon activation, they release a wide spectrum of factors responsible for modulating inflammation, extracellular matrix (ECM) remodeling, and tissue repair.
The study aimed to characterize the astrocytic secretome under post-ischemic conditions and to identify mechanisms regulating the expression and secretion of ECM-related proteins and, most importantly - CHI3L1.
To investigate the astrocytic secretome after stroke, we combined an in vitro model mimicking post-stroke astrocyte activation with mass-spectrometry analyses. Key findings were validated using an in vivo stroke model in mice as well as various in vitro strategies for astrocyte activation.
Proteomic profiling revealed a strong enrichment in ECM-related proteins and elevated levels of CHI3L1 in the secretome of activated astrocytes. Subsequent analyses demonstrated that TGFβ and proinflammatory factors such as IL1β and TNFα upregulate CHI3L1 expression and secretion in astrocytes.
Our ultimate goal is to define how factors secreted by astrocytes not only shape the brain microenvironment, but also influence regeneration and recovery after stroke. The results obtained so far indicate that CHI3L1 is a dynamically regulated component of the reactive astrocytes secretome with its expression and secretion upregulated by TGFβ and pro-inflammatory cytokines.
