scispace - formally typeset
L

Laura Calzà

Researcher at University of Bologna

Publications -  244
Citations -  8045

Laura Calzà is an academic researcher from University of Bologna. The author has contributed to research in topics: Neuropeptide & Receptor. The author has an hindex of 47, co-authored 230 publications receiving 7336 citations. Previous affiliations of Laura Calzà include University of Cagliari & Health Science University.

Papers
More filters
Journal ArticleDOI

GM1 ganglioside stimulates the regeneration of dopaminergic neurons in the central nervous system.

TL;DR: The effect of GM1 ganglioside on the recovery of nigro-strital dopaminergic neurons was studied in rats after unilateral hemitransection and it is found that repeated administration ofGM1 significantly increased the HVA content, the tyrosine hydroxylase activity and the tyosine hydoxylase-related immunofluorescence in the striatum ipsilateral to the lesion.
Journal ArticleDOI

Gangliosides increase the survival of lesioned nigral dopamine neurons and favour the recovery of dopaminergic synaptic function in striatum of rats by collateral sprouting.

TL;DR: It is introduced that following ganglioside treatment some lesioned DA nerve cells do not degenerate, but elongate their dendrites to give increased trophic support to DA cell bodies with intact DA axons, and may possibly represent a new type of drug in the treatment of Parkinson's disease and aging processes in DA systems.
Journal ArticleDOI

Nerve growth factor control of neuronal expression of angiogenetic and vasoactive factors.

TL;DR: The present investigation suggests that the increase of scg size induced by NGF and 6-OHDA + NGF is associated with neoangiogenesis, and that the induction of vasoactive and angiogenic factors in neurons represents a further and previously undisclosed effect of NGF.
Journal ArticleDOI

Early Pharmacotherapy Restores Neurogenesis and Cognitive Performance in the Ts65Dn Mouse Model for Down Syndrome

TL;DR: Results show that early pharmacotherapy with a drug usable by humans can correct neurogenesis and behavioral impairment in a model for DS, and that proliferation was completely rescued by fluoxetine.