Lab
Laboratory of Developmental Neurobiology
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Statement of Research Interest
Our research focuses on the study of Danio rerio (zebrafish), one of the most commonly used vertebrate models in biomedical research. We employ both embryonic and adult zebrafish to investigate neurodegenerative diseases and cancer.
In our laboratory, we have recently implemented zebrafish as an in vivo model for studying Alexander disease (AxD) (1,2) a rare, autosomal dominant neurodegenerative condition caused by heterozygous mutations in the gene encoding glial fibrillary acidic protein (GFAP). These mutations compromise the filamentous architecture of GFAP in astrocytes, leading to the accumulation of toxic protein aggregates. AxD is marked by disrupted axonal myelination, likely stemming from incomplete maturation of oligodendrocytes-cells essential for effective signal transmission due to their role in forming the myelin sheath. Currently, there is no cure for AxD, and available treatments are limited to symptomatic relief. Using microinjection combined with Tol2 transgenesis, we developed a transgenic zebrafish line that expresses the mutant human form of GFAP. This model displays typical aggregate formation, thereby confirming the utility of zebrafish as a valuable platform for investigating Alexander disease.
1: Bellitto D, Bozzo M, Ravera S, Bertola N, Rosamilia F, Milia J, Barboro P, Vargas GC, Di Lisa D, Pastorino L, Lantieri F, Castagnola P, Iervasi E, Ponassi M, Profumo A, Tkachenko K, Rosano C, Candiani S, Bachetti T. A multi-omics approach reveals impaired lipid metabolism and oxidative stress in a zebrafish model of Alexander disease.
In our laboratory, we have recently implemented zebrafish as an in vivo model for studying Alexander disease (AxD) (1,2) a rare, autosomal dominant neurodegenerative condition caused by heterozygous mutations in the gene encoding glial fibrillary acidic protein (GFAP). These mutations compromise the filamentous architecture of GFAP in astrocytes, leading to the accumulation of toxic protein aggregates. AxD is marked by disrupted axonal myelination, likely stemming from incomplete maturation of oligodendrocytes-cells essential for effective signal transmission due to their role in forming the myelin sheath. Currently, there is no cure for AxD, and available treatments are limited to symptomatic relief. Using microinjection combined with Tol2 transgenesis, we developed a transgenic zebrafish line that expresses the mutant human form of GFAP. This model displays typical aggregate formation, thereby confirming the utility of zebrafish as a valuable platform for investigating Alexander disease.
1: Bellitto D, Bozzo M, Ravera S, Bertola N, Rosamilia F, Milia J, Barboro P, Vargas GC, Di Lisa D, Pastorino L, Lantieri F, Castagnola P, Iervasi E, Ponassi M, Profumo A, Tkachenko K, Rosano C, Candiani S, Bachetti T. A multi-omics approach reveals impaired lipid metabolism and oxidative stress in a zebrafish model of Alexander disease.
Lab Members
| Bazzurro, Virginia Post-Doc | Matteo, Bozzo Post-Doc |