NICO NeuroWebinar

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Data dell'evento: dal 20/05/2022 al 20/05/2022


1 appointment per week, on Friday at 2.00 pm

20/5/22 h. 2:00 pm  - Progress report
Sara Bonzano (Group Bonfanti-Peretto)
A Pilot Investigation of Nr2f1 expression and functions during Experience-dependent Neuroplasticity in the Adult Mouse Dentate Gyrus

webex link

13/5/22 h. 2:00 pm  - Webinar
Stefano Zucca (Group Peretto - Bonfanti)
Breaking the stigma on Academic Mental Health

In the past 10 years there has been an increased attention on mental health and wellbeing among people working in academia. A wide range of scientific papers, local and global surveys together with articles and commentaries highlight a worrying situation about mental health issues among PhD students and early career researchers. Long working hours, competition, job insecurity and toxic working environments are causing extremely high stress levels in academia. Recent evidence shows that nearly 20% of PhD students suffer from diagnosable anxiety or depression. In this talk, I will provide an overview of what we know about mental health and wellbeing in academia, focusing on common stressors among researchers. I will cover main factors contributing to high stress levels in academic working environments and I will propose possible solutions to manage researchers’ stress and improve their wellbeing. Discussing and raising awareness about mental health in academia is a fundamental step to fight stigma and help people seeking help, if and when they need.

6/5/22 h. 2:00 pm  - Progress report
Martina Lorenzati (Group Buffo)
Human IPSCs-derived oligodendrocytes and astrocytes as the first Autosomal Dominant Leukodystrophy-relevant cellular models

22/4/22 h. 2:00 pm  - Progress report
Giovanna Menduti (Group Vercelli)
Moxifloxacin rescues Spinal Muscular Atrophy phenotypes in both animal model and patient-derived cells

14/4/22 h. 2:00 pm  - Progress report
Gianmarco Pallavicini (Group Di Cunto)
Human and mice neurodevelopment, how models change findings

1/4/22 h. 4:00 pm  - Lecture
  Shi-Bin Li, Stanford University

Interrogation of sleep disorders associated with aging and stress
We spend approximately a third of our lives asleep. High-quality sleep is essential to maintain our physical and mental health. A good night sleep not only restores our physical and mental strength efficiently, but also helps us to maintain mental health and strengthen immunity. However, sleep is subjected to various challenges including aging and stress, across the lifespan. Sleep quality declines with age. The elderly usually experience low-quality sleep including difficulty to fall asleep, reduction in slow-wave/deep sleep, early waking up, and prominently sleep fragmentation which heavily impairs the ability of sleep in restoring physical and mental strength. Stress not only prevents us from a good night slumber, but may also make us more vulnerable to pathogen exposure. Around these topics, Dr. Li and colleagues accumulated some evidence showing a mechanistic underpinning of sleep instability with age, and a hypothalamic circuitry underlying stress-induced hyperarousal/insomnia and peripheral immunosuppression.
Host: Ilaria Bertocchi 

18/3/22 h. 4:00 pm  - Lecture
  Dilek Colak, Ph.D.
Assistant Professor of Neuroscience, Feil Family Brain and Mind Institute, Center for Neurogenetics
Assistant Professor of Pediatrics, Gale and Ira Drukier Institute for Children's Health
Weill Medical College, Cornell University, New York

Astrocyte dysfunction in ASD
The cellular mechanisms of autism spectrum disorder (ASD) are poorly understood. Cumulative evidence suggests that abnormal synapse function underlies many features of this disease. Astrocytes regulate several key neuronal processes, including the formation of synapses and the modulation of synaptic plasticity. Astrocyte abnormalities have also been identified in the postmortem brain tissue of ASD individuals. To address this, we combined stem cell culturing with transplantation techniques and demonstrated that astrocytes derived from ASD iPSCs are sufficient to induce repetitive behavior as well as cognitive deficit in experimental animals, suggesting a previously unrecognized primary role for astrocytes in ASD.
Host: Annalisa Buffo 

11/3/22 h. 2:00 pm  - Progress report
Gabriela Berenice Gomez Gonzalez (Group Buffo)
Assessing the functional integration of hESC-derived striatal grafts in a rat model of HD by calcium photometry

4/3/22 h. 2:00 pm  - Lecture
  Angelo Forli, Ph.D.
Department of Bioengineering, University of California, Berkeley

Collective behavior and hippocampal activity in freely foraging bats
Social and collective behaviors are widespread across the animal kingdom, from ants to humans. Despite their prevalence and their role in shaping brain evolution, the neurobiological bases of collective behaviors remain largely unexplored. I will describe how I am attempting to address this challenge by (1) monitoring a group of Egyptian Fruit bats – highly social mammals – collectively foraging in a large laboratory room and (2) by recording the activity of single neurons in their hippocampus, a fundamental brain region for navigating physical and social space.
Host: Serena Bovetti

25/2/22 h. 2:00 pm  - Progress report
Ilaria Bertocchi (Group Eva)
Role of perineuronal nets in fragile X syndrome

Thursday 24/2/22 h. 2:00 pm  - Internal Seminar, Group Buffo
Ben Vermaercke, Postdoctoral researcher  
VIB-KU Leuven Center for Brain & Disease Research, Leuven Brain Institute, Belgium

Probing functional outputs of human transplanted neurons in mouse visual circuits

Host: Gabriela B. Gómez-González  

18/2/22 - Lecture
  Alessandro Bertero, PhD
Armenise-Harvard Lab of Heart Engineering and Developmental Genomics
Molecular Biotechnology Center, University of Turin
Department of Molecular Biotechnology and Health Sciences

Functional dynamics of chromatin topology in human cardiogenesis and disease

Recent technological advancements in the field of chromatin biology have rewritten the textbook on nuclear organization. We now appreciate that the folding of chromatin in the three-dimensional space (i.e. its 3D “architecture”) is non-random, hierarchical, and highly complex. Nevertheless, functional changes in spatial genome organization during human development or disease remain poorly understood. We have investigated these dynamics in two models: (1) the differentiation of human pluripotent stem cells into cardiomyocytes (hPSC-CM); (2) hPSC-CM from patients with cardiac laminopathy, a genetic dilated cardiomyopathy with severe conduction disease due to mutations in the LMNAgene. We combined omics methods to probe nuclear structure (Hi-C), chromatin accessibility (ATAC-seq), and gene expression (RNA-seq), genetic perturbations by CRISPR/Cas9, and cardiac physiology assays. In this seminar I will summarize our published findings and present novel preliminary data that indicate the dynamic nature of genome organization during human development and disease, and show how these spatial relationships can regulate lineage-specific gene expression. Finally, I will describe the methods we are developing to probe the structure-function relationship of chromatin.

Host: Annalisa Buffo
webex link 

11/2/22 - Progress report
  Maryam Khastkhodaei Ardakani (Group Buffo)
​Rescuing neural cell survival and maturation in a microcephaly 17 (MCPH17) model: effects of postnatal and in utero N-acetyl cysteine treatments

4/2/22 - Progress report
  Francesca Montarolo (Group Capobianco)
​Age- and sex-dependent behavioral phenotypes in NURR1 deficient mice

28/1/22 - Lecture
  Giulia Ramazzotti, PhD
Department of Biomedical and Neuromotor Sciences, University of Bologna

​Cell signaling pathways in autosomal-dominant leukodystrophy (ADLD): the intriguing role of the astrocytes

Autosomal-dominant leukodystrophy (ADLD) is an extremely rare fatal neurodegenerative disorder due to the overexpression of the nuclear lamina component, Lamin B1.The molecular mechanisms responsible for driving the onset and development of this pathology are not clear yet. Vacuolar demyelination seems to be one of the most significant histopathological observations of ADLD.
Considering the role of oligodendrocytes, astrocytes, and leukemia inhibitory factor (LIF)-activated signaling pathways in the myelination processes, we analyzed signaling alterations in different cell populations from patients with LMNB1 duplications and cellular models overexpressing Lamin B1 protein. Our results point out, for the first time, that astrocytes may be pivotal in the evolution of the disease. Indeed, cells from ADLD patients and astrocytes overexpressing LMNB1 show severe ultrastructural nuclear alterations, not present in oligodendrocytes overexpressing LMNB1. Moreover, the accumulation of Lamin B1 in astrocytes induces a reduction in LIF and in LIF-receptor levels with a consequential downregulation of downstream signaling pathways. Significantly, the toxic effects induced by Lamin B1 accumulation can be partially reversed, with differences between astrocytes and oligodendrocytes, highlighting that LMNB1 overexpression drastically affects astrocytic function reducing their fundamental support to oligodendrocytes in the myelination process. In addition, astrocytes overexpressing Lamin B1 show increased immunoreactivity for both GFAP and vimentin and also an increase in NF-kB phosphorylation and c-Fosactivation, suggesting the induction of astrocytes reactivity.
Therefore, Lamin B1 accumulation correlates with biochemical, metabolic, and morphologic remodeling, probably related to the induction of a reactive astrocytes phenotype that could be directly associated to ADLD pathological mechanisms.

Host: Annalisa Buffo

21/1/22 - Progress report
  Roberta Schellino (Group Vercelli)
Long-term transplantation and enriched environment favor human striatal progenitor maturation and functional recovery in a rat model of Huntington’s Disease

14/1/22 - Progress report
  Brigitta Bonaldo (Group Panzica)
Effects of perinatal exposure to bisphenol A or S in EAE model of multiple sclerosis.


20 maggio 2022


Esposizione cronica al bisfenolo A in gravidanza: come le plastiche possono alterare encefalo e comportamento sociale

L’esposizione cronica per un periodo che copre gravidanza e allattamento, a una dose di BPA pari a quella indicata come dose tollerabile giornaliera (TDI) dall’EFSA (European Food Safety Authority) causa nelle femmine di topo alterazioni sia a livello comportamentale che encefalico.
I risultati dello studio realizzato dai nostri ricercatori del gruppo di Neuroendocrinologia e pubblicati sull’European Journal of Histochemistry suggeriscono quanto sia urgente adottare misure più stringenti nell'utilizzo di BPA, a tutela della salute di tutti.  

12 gennaio 2022