Giorgia Migliorato
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Giorgia Migliorato has a total of 10 co-authors. Here are the top co-authors by number of shared publications:
- Emanuela Paldino
Laboratory of Neuroanatomy, Fondazione Santa Lucia IRCCS, 00143 Rome, Italy
1 shared publication - Ezia Guatteo
Laboratorio di Neurologia Sperimentale, Fondazione Santa Lucia IRCCS, Rome, Italy
1 shared publication - Francesca Romana Fusco
Laboratory of Neuroanatomy, Fondazione Santa Lucia IRCCS, Rome, Italy
1 shared publication - Giuseppe Sancesario
Department of Systems Medicine, University of Rome Tor Vergata, 00133 Rome, Italy
1 shared publication - Mariangela Massaro Cenere
Neuroscienze Sperimentali, IRCCS Fondazione Santa Lucia, Rome, Italy
1 shared publication - Nicola Berretta
Department of Experimental Neuroscience, Santa Lucia Foundation IRCCS, Rome, Italy
1 shared publication
Latest Publications
- Open Access
- 4 September 2022
- Published by MDPI AG in International Journal of Molecular Sciences
- Vol. 23 (17) , 10126
Neuropathology of the Basal Ganglia in SNCA Transgenic Rat Model of Parkinson’s Disease: Involvement of Parvalbuminergic Interneurons and Glial-Derived Neurotropic Factor
Parkinson’s disease (PD) is a neurodegenerative disease characterized by the accumulation of alpha-synuclein, encoded by the SNCA gene. The main neuropathological hallmark of PD is the degeneration of dopaminergic neurons leading to striatal dopamine depletion. Trophic support by a neurotrophin called glial-derived neurotrophic factor (GDNF) is also lacking in PD. We performed immunohistochemical studies to investigate neuropathological changes in the basal ganglia of a rat transgenic model of PD overexpressing alfa-synuclein. We observed that neuronal loss also occurs in the dorsolateral part of the striatum in the advanced stages of the disease. Moreover, along with the degeneration of the medium spiny projection neurons, we found a dramatic loss of parvalbumin interneurons. A marked decrease in GDNF, which is produced by parvalbumin interneurons, was observed in the striatum and in the substantia nigra of these animals. This confirmed the involvement of the striatum in the pathophysiology of PD and the importance of GDNF in maintaining the health of the substantia nigra.
- 4 September 2022
- Published by MDPI AG in International Journal of Molecular Sciences
- Vol. 23 (17) , 10126
Open AccessNeuropathology of the Basal Ganglia in SNCA Transgenic Rat Model of Parkinson’s Disease: Involvement of Parvalbuminergic Interneurons and Glial-Derived Neurotropic Factor
Parkinson’s disease (PD) is a neurodegenerative disease characterized by the accumulation of alpha-synuclein, encoded by the SNCA gene. The main neuropathological hallmark of PD is the degeneration of dopaminergic neurons leading to striatal dopamine depletion. Trophic support by a neurotrophin called glial-derived neurotrophic factor (GDNF) is also lacking in PD. We performed immunohistochemical studies to investigate neuropathological changes in the basal ganglia of a rat transgenic model of PD overexpressing alfa-synuclein. We observed that neuronal loss also occurs in the dorsolateral part of the striatum in the advanced stages of the disease. Moreover, along with the degeneration of the medium spiny projection neurons, we found a dramatic loss of parvalbumin interneurons. A marked decrease in GDNF, which is produced by parvalbumin interneurons, was observed in the striatum and in the substantia nigra of these animals. This confirmed the involvement of the striatum in the pathophysiology of PD and the importance of GDNF in maintaining the health of the substantia nigra.