Early bioenergetic changes and altered neuronal excitability in a rodent model of prodromal Parkinson's disease

Abstract: Parkinson’s disease (PD) is closely related to mitochondrial dysfunction, but it is unclear how early metabolic alterations affect neuronal function before obvious neurodegeneration. We investigated male PTEN-induced kinase 1 mice at postnatal days 30 and 60 using a multidisciplinary approach integrating behavioural, proteomic, bioenergetic, skeletal-muscle and electrophysiological analyses. Motor performance showed subtle age-dependent alterations, whereas sensorimotor function remained largely preserved despite age- and region-dependent molecular remodelling within the nigrostriatal system. On postnatal day 60, dorsal striatal tissue showed increased respiratory reserve, while skeletal muscle developed a more oxidative phenotype. In parallel, striatal neurons showed age-dependent hypoexcitability with a Glibenclamide-sensitive component, whereas nigral dopaminergic neurons showed altered depolarisation-evoked Ca²⁺ responses. These findings indicate that early PINK1 deficiency is characterised by age- and region-dependent metabolic and functional adaptation rather than generalised mitochondrial failure, consistent with bioenergetic remodelling as a feature of early PINK1-associated pathology

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Publication Details

Journal
Zenodo (CERN European Organization for Nuclear Research)
Published
2026-10-29
DOI
https://doi.org/10.5281/zenodo.23760538
Primary Topic
Parkinson's Disease Mechanisms and Treatments
Type
article
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article

Early bioenergetic changes and altered neuronal excitability in a rodent model of prodromal Parkinson's disease

Victor Corasolla Carregari, Giuseppina Martella, Martina Montanari, Valentina Nesci et al.
Zenodo (CERN European Organization for Nuclear Research)
Parkinson's Disease Mechanisms and Treatments
article

Early bioenergetic changes and altered neuronal excitability in a rodent model of prodromal Parkinson's disease

Victor Corasolla Carregari, Giuseppina Martella, Martina Montanari, Valentina Nesci, Cristiana Valle, Silvia Scaricamazza, Antonella Peppe, Ezia Guatteo, Cecilia Giacomet, Maria Meringolo, Nicola Biagio Mercuri, Luisa Pieroni, Sebastian Luca D’Addario, Paola Bonsi, Annalisa Tassone, Beatrice Zarrillli
article en

Abstract

Abstract: Parkinson’s disease (PD) is closely related to mitochondrial dysfunction, but it is unclear how early metabolic alterations affect neuronal function before obvious neurodegeneration. We investigated male PTEN-induced kinase 1 mice at postnatal days 30 and 60 using a multidisciplinary approach integrating behavioural, proteomic, bioenergetic, skeletal-muscle and electrophysiological analyses. Motor performance showed subtle age-dependent alterations, whereas sensorimotor function remained largely preserved despite age- and region-dependent molecular remodelling within the nigrostriatal system. On postnatal day 60, dorsal striatal tissue showed increased respiratory reserve, while skeletal muscle developed a more oxidative phenotype. In parallel, striatal neurons showed age-dependent hypoexcitability with a Glibenclamide-sensitive component, whereas nigral dopaminergic neurons showed altered depolarisation-evoked Ca²⁺ responses. These findings indicate that early PINK1 deficiency is characterised by age- and region-dependent metabolic and functional adaptation rather than generalised mitochondrial failure, consistent with bioenergetic remodelling as a feature of early PINK1-associated pathology

Zenodo (CERN European Organization for Nuclear Research)
University of Rome Tor Vergata (IT), Università Campus Bio-Medico (IT), Parthenope University of Naples (IT), Agostino Gemelli University Polyclinic (IT), Saint Camillus International University of Health and Medical Sciences (IT), Pegaso University (IT), Fondazione Santa Lucia (IT), National Research Council (IT)
Good health and well-being
Openalex Percentile: Top 14%
Parkinson's Disease Mechanisms and Treatments
DOIOpen Access PDFOpenAlex
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