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Molecular Neuroscience and Pharmacology

Research group

Active research

Project owner

Institute for Neuroscience and Physiology

Area

Health and medicine

Topic

Neurosciences Pharmacology and Toxicology

Short description

Our research explores the complex interactions between the dopaminergic system and neural circuits regulated by dopamine signaling, with a particular focus on the basal ganglia. We aim to uncover how disruptions in these pathways contribute to neurological disorders, including autism spectrum disorders (ASD), and to develop innovative therapeutic strategies.

Research interest

Our research aims to understand the molecular mechanisms that underlie dysfunctions in specific brain circuitries within the basal ganglia system. We aim to elucidate how dopamine influences motor control, cognitive function, and emotional regulation, as well as how protein synthesis within neurons supports these processes. The interdisciplinary approach we adopt integrates a variety of advanced techniques—including molecular biology, rodent behavioral studies, electrophysiology, confocal imaging, and genetics.

Our primary research focuses on neurodevelopmental disorders, such as autism spectrum disorders (ASD) and fragile X syndrome (FXS), as well as neurodegenerative diseases like Parkinson's disease (PD). We investigate how dysregulation of protein synthesis affects synaptic function, neuronal connectivity, and behavior, aiming to uncover fundamental mechanisms of brain function and the pathological changes underlying these conditions.

Our findings have broad implications for understanding disease pathophysiology and developing potential therapeutic strategies.

Ongoing research

Our group is currently investigating the complex relationship between ASD and its comorbidities. ASD is frequently associated with a range of psychiatric and somatic conditions, which can further exacerbate the challenges faced by affected individuals.

A current project in our lab explores how dysregulated protein synthesis and molecular signaling pathways in the basal ganglia contribute to disrupted eating behavior in fragile X syndrome (FXS), the leading genetic cause of ASD. One promising avenue of investigation is the role of the striatum, a brain region involved in regulating compulsive-like behaviors, including food-seeking and consumption. Diet-induced obesity, the most common form of obesity, is characterized by compulsive overeating, impaired inhibitory control, and negative emotionality—features frequently observed in individuals with ASD.

By identifying the neural and molecular mechanisms underlying these behavioral alterations, we aim to advance our understanding of ASD-related eating dysfunctions and uncover potential therapeutic targets.

none — Immunofluorescent detection of TH+ (green) neurons and PERK (red) expression in SNc and VTA dopaminergic neurons of PERKf/f DAT-Cre and WT DAT-Cre mice.

Adapted from Longo F, et al. "Cell-type-specific disruption of PERK-eIF2α signaling in dopaminergic neurons alters motor and cognitive function." Molecular psychiatry 26.11 (2021): 6427-6450. doi: 10.1038/s41380-021-01099-w

Group members

Francesco Longo, PhD, Group Leader
Lindsay Zentveld, Research assistant (part-time)
Ching Yu Suen, Bachelor student
Sarah Sundström, Master student (Umeå universitet)
Ranim Aboalaenen, Master student
Meriem Al-Muweyel, Master student
Saly Alsyah, Master student

Francesco Longo is the group leader at the Department of Pharmacology. He obtained his PhD in Pharmacology at the University of Ferrara (Italy) and performed his postdoctoral training at New York University (USA) and at the University of Gothenburg.