In the recent past, the pathogenesis of Parkinson's disease (PD) has evolved from a neurodegenerative disorder considered entirely sporadic to a disease with an unequivocal genetic component. Indeed, different inherited forms of PD have been discovered and characterized, although the functional roles of the gene products identified are still under intense investigation. To gain a better understanding of the cellular and molecular pathogenic mechanisms of hereditary forms of PD, different animal models have been generated. Although most of the rodent models display neither obvious behavioral impairment nor evidence for neurodegeneration, remarkable abnormalities of dopamine-mediated neurotransmission and corticostriatal synaptic plasticity have been described, indicative of a fundamental distortion of network function within the basal ganglia. The picture emerging from a critical review of recent data on monogenic parkinsonisms suggests that mutations in PD genes might cause developmental rearrangements in the corticobasal ganglia circuitry, compensating the dopaminergic dysfunction observed both in mice and humans, in order to maintain proper motor function.

Madeo, G., Martella, G., Schirinzi, T., Ponterio, G., Shen, J., Bonsi, P., et al. (2012). Aberrant striatal synaptic plasticity in monogenic parkinsonisms. NEUROSCIENCE, 211, 126-135 [10.1016/j.neuroscience.2011.07.065].

Aberrant striatal synaptic plasticity in monogenic parkinsonisms

MADEO, GRAZIELLA;MARTELLA, GIUSEPPINA;PISANI, ANTONIO
2012-06-01

Abstract

In the recent past, the pathogenesis of Parkinson's disease (PD) has evolved from a neurodegenerative disorder considered entirely sporadic to a disease with an unequivocal genetic component. Indeed, different inherited forms of PD have been discovered and characterized, although the functional roles of the gene products identified are still under intense investigation. To gain a better understanding of the cellular and molecular pathogenic mechanisms of hereditary forms of PD, different animal models have been generated. Although most of the rodent models display neither obvious behavioral impairment nor evidence for neurodegeneration, remarkable abnormalities of dopamine-mediated neurotransmission and corticostriatal synaptic plasticity have been described, indicative of a fundamental distortion of network function within the basal ganglia. The picture emerging from a critical review of recent data on monogenic parkinsonisms suggests that mutations in PD genes might cause developmental rearrangements in the corticobasal ganglia circuitry, compensating the dopaminergic dysfunction observed both in mice and humans, in order to maintain proper motor function.
1-giu-2012
Pubblicato
Rilevanza internazionale
Articolo
Esperti anonimi
Settore MED/26 - NEUROLOGIA
English
Con Impact Factor ISI
Animals; Neural Pathways; Corpus Striatum; Disease Models, Animal; Parkinsonian Disorders; Models, Neurological; Homeostasis; Neuronal Plasticity; Dopaminergic Neurons; Synaptic Transmission
Madeo, G., Martella, G., Schirinzi, T., Ponterio, G., Shen, J., Bonsi, P., et al. (2012). Aberrant striatal synaptic plasticity in monogenic parkinsonisms. NEUROSCIENCE, 211, 126-135 [10.1016/j.neuroscience.2011.07.065].
Madeo, G; Martella, G; Schirinzi, T; Ponterio, G; Shen, J; Bonsi, P; Pisani, A
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2108/88270
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