Axon demyelination and degeneration in a zebrafish spastizin model of hereditary spastic paraplegia DOI Creative Commons
Vranda Garg,

Selina André,

Luisa Heyer

и другие.

Open Biology, Год журнала: 2024, Номер 14(11)

Опубликована: Ноя. 1, 2024

Hereditary spastic paraplegias (HSPs) are a diverse set of neurological disorders characterized by progressive spasticity and weakness in the lower limbs caused damage to axons corticospinal tract. More than 88 genetic mutations have been associated with HSP, yet mechanisms underlying these not well understood. We replicated pathophysiology one form HSP known as paraplegia 15 (SPG15) zebrafish. This disorder is humans ZFYVE26 gene, which codes for protein called SPASTIZIN. show that, zebrafish, significant reduction Spastizin degeneration large motor neurons. Motor neuron axon demyelination spinal cord impaired locomotion spastizin mutants. Our findings reveal that compromises axonal integrity affects myelin sheath, ultimately recapitulating HSPs.

Язык: Английский

Effect of High Glucose on Embryological Development of Zebrafish, Brachyodanio, Rerio through Wnt Pathway DOI Open Access

Ebony Thompson,

Justin Hensley,

Renfang Song Taylor

и другие.

International Journal of Molecular Sciences, Год журнала: 2024, Номер 25(17), С. 9443 - 9443

Опубликована: Авг. 30, 2024

Gestational diabetes mellitus (GDM) is a worldwide pregnancy complication. can significantly impact fetus development. However, the effects of high glucose on embryological development post-fertilization are yet to be researched. Danio rerio embryos great model for studying embryonic In this study, (morphological and genetic) were examined in presence high-glucose environment that mimics developing pregnant women with GDM. Fertilized zebrafish treated normal media 5 days from 3 h (hpf) 96 hpf, respectively, as control experimental groups. Morphological changes recorded microscope images. Hatch rate heart compared between groups at set time points. RNA-Seq performed examine gene group. Glucose delayed embryo by slowing hatch about 24 h. The brain, heart, tail started showing smaller morphology group hpf. Heart was faster 2 statistically significant difference. Among whole genome, changed genes 556 upregulated 1118 downregulated genes, metabolic Wnt pathways altered under conditions. These conditions contribute physiological differences may provide insight into functionality post-embryological

Язык: Английский

Процитировано

0
Axon demyelination and degeneration in a zebrafish spastizin model of hereditary spastic paraplegia DOI Creative Commons
Vranda Garg,

Selina André,

Luisa Heyer

и другие.

Open Biology, Год журнала: 2024, Номер 14(11)

Опубликована: Ноя. 1, 2024

Hereditary spastic paraplegias (HSPs) are a diverse set of neurological disorders characterized by progressive spasticity and weakness in the lower limbs caused damage to axons corticospinal tract. More than 88 genetic mutations have been associated with HSP, yet mechanisms underlying these not well understood. We replicated pathophysiology one form HSP known as paraplegia 15 (SPG15) zebrafish. This disorder is humans ZFYVE26 gene, which codes for protein called SPASTIZIN. show that, zebrafish, significant reduction Spastizin degeneration large motor neurons. Motor neuron axon demyelination spinal cord impaired locomotion spastizin mutants. Our findings reveal that compromises axonal integrity affects myelin sheath, ultimately recapitulating HSPs.

Язык: Английский

Процитировано

0