Explore the words cloud of the SynapticMitochondria project. It provides you a very rough idea of what is the project "SynapticMitochondria" about.
The following table provides information about the project.
INSTITUTO DE MEDICINA MOLECULAR JOAO LOBO ANTUNES
|Coordinator Country||Portugal [PT]|
|Total cost||1˙300˙000 €|
|EC max contribution||1˙300˙000 € (100%)|
1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
|Duration (year-month-day)||from 2016-09-01 to 2021-08-31|
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|1||INSTITUTO DE MEDICINA MOLECULAR JOAO LOBO ANTUNES||PT (LISBOA)||coordinator||1˙300˙000.00|
Mitochondria at the synapse have a pivotal role in neurotransmitter release, but almost nothing is known about synaptic mitochondria composition or specific functions. Synaptic mitochondria compared to mitochondria in other cells, need to cope with increased calcium load, more oxidative stress, and high demands of energy generation during synaptic activity. My hypothesis is that synaptic mitochondria have acquired specific mechanisms to manage local stress and that disruption of these mechanisms contributes to neurodegeneration. How mitochondria sense their dysfunction is unclear. Even more intriguing is the question how they decide whether their failure should lead to removal of the organelle or dismissal of the complete neuron via cell death. We anticipate that these decisions are not only operational during disease, but might constitute a fundamental mechanism relevant for maintenance of synaptic activity and establishment of new synapses. Recent studies have revealed several genes implicated in neurodegenerative disorders involved in mitochondrial maintenance. However the function of these genes at the synapse, where the initial damage occurs, remains to be clarified. These genes provide excellent starting points to decipher the molecular mechanisms discussed above. Furthermore I propose to use proteomic approaches to identify the protein fingerprint of synaptic mitochondria and to compare them to mitochondria from other tissues. I plan to identify key players of the proposed regulatory pathways involved in intrinsic mitochondria quality control. In a complimentary approach, I will exploit our findings and use in vitro and in vivo experimental approaches to measure mitochondrial function of synaptic versus non-synaptic mitochondria and the relevance of those changes for synaptic function. Our work will unravel the specific properties of synaptic mitochondria and provide much needed insight in their hypothesized predominant role in neurodegenerative disorders.
|year||authors and title||journal||last update|
Marco Spinazzi, Enrico Radaelli, Katrien HorrÃ©, Amaia M. Arranz, Natalia V. Gounko, Patrizia Agostinis, Teresa Mendes Maia, Francis Impens, Vanessa Alexandra Morais, Guillermo Lopez-Lluch, Lutgarde Serneels, Placido Navas, Bart De Strooper
PARL deficiency in mouse causes Complex III defects, coenzyme Q depletion, and Leigh-like syndrome
published pages: 277-286, ISSN: 0027-8424, DOI: 10.1073/pnas.1811938116
|Proceedings of the National Academy of Sciences 116/1||2019-06-06|
Melissa Vos, Ann Geens, Claudia BÃ¶hm, Liesbeth Deaulmerie, Jef Swerts, Matteo Rossi, Katleen Craessaerts, Elvira P. Leites, Philip Seibler, Aleksandar Rakovic, Thora Lohnau, Bart De Strooper, Sarah-Maria Fendt, Vanessa A. Morais, Christine Klein, Patrik Verstreken
Cardiolipin promotes electron transport between ubiquinone and complex I to rescue PINK1 deficiency
published pages: 695-708, ISSN: 0021-9525, DOI: 10.1083/jcb.201511044
|The Journal of Cell Biology 216/3||2019-06-06|
Elvira P. Leites, Vanessa A. Morais
Mitochondrial quality control pathways: PINK1 acts as a gatekeeper
published pages: 45-50, ISSN: 0006-291X, DOI: 10.1016/j.bbrc.2017.06.096
|Biochemical and Biophysical Research Communications 500/1||2019-06-06|
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