neurons rely on mitochondrial energy metabolism for essential functions like neurogenesis, neurotransmission, and synaptic plasticity. mitochondrial dysfunctions are associated with neurodevelopmental disorders including fragile X syndrome (FXS), the most common cause of inherited intellectual disability, which also presents with motor skill deficits. however, the precise role of mitochondria in the pathophysiology of FXS remains largely unknown. notably, previous studies have linked the serotonergic system and mitochondrial activity to FXS. our study investigates the potential therapeutic role of serotonin receptor 1A (5-HT1A) in FXS. using the drosophila model of FXS, we demonstrated that treatment with eltoprazine, a 5-HT1A agonist, can ameliorate synaptic transmission, correct mitochondrial deficits, and ultimately improve motor behavior. while these findings suggest that the 5-HT1A-mitochondrial axis may be a promising therapeutic target, further investigation is needed in the context of FXS.

Vannelli, A., Mariano, V., Bagni, C., Kanellopoulos, A.k. (2024). Activation of the 5-HT1A Receptor by Eltoprazine Restores Mitochondrial and Motor Deficits in a Drosophila Model of Fragile X Syndrome. INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, 25(16) [10.3390/ijms25168787].

Activation of the 5-HT1A Receptor by Eltoprazine Restores Mitochondrial and Motor Deficits in a Drosophila Model of Fragile X Syndrome

Bagni, Claudia;
2024-01-01

Abstract

neurons rely on mitochondrial energy metabolism for essential functions like neurogenesis, neurotransmission, and synaptic plasticity. mitochondrial dysfunctions are associated with neurodevelopmental disorders including fragile X syndrome (FXS), the most common cause of inherited intellectual disability, which also presents with motor skill deficits. however, the precise role of mitochondria in the pathophysiology of FXS remains largely unknown. notably, previous studies have linked the serotonergic system and mitochondrial activity to FXS. our study investigates the potential therapeutic role of serotonin receptor 1A (5-HT1A) in FXS. using the drosophila model of FXS, we demonstrated that treatment with eltoprazine, a 5-HT1A agonist, can ameliorate synaptic transmission, correct mitochondrial deficits, and ultimately improve motor behavior. while these findings suggest that the 5-HT1A-mitochondrial axis may be a promising therapeutic target, further investigation is needed in the context of FXS.
2024
Pubblicato
Rilevanza internazionale
Articolo
Esperti anonimi
Settore BIOS-10/A - Biologia cellulare e applicata
English
intellectual disability
synaptic transmission
serotonin
neuromuscular junction
FXS therapy
eltoprazine
Vannelli, A., Mariano, V., Bagni, C., Kanellopoulos, A.k. (2024). Activation of the 5-HT1A Receptor by Eltoprazine Restores Mitochondrial and Motor Deficits in a Drosophila Model of Fragile X Syndrome. INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, 25(16) [10.3390/ijms25168787].
Vannelli, A; Mariano, V; Bagni, C; Kanellopoulos, Ak
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2108/388997
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