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Tau depletion in human neurons mitigates Aβ-driven toxicity.
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Hyperexcitability in young iPSC-derived C9ORF72 mutant motor neurons is associated with increased intracellular calcium release.
Scientific Reports
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Mancini, Andrea, Mazzocchetti, Petra, Sciaccaluga, Miriam, Megaro, Alfredo, Bellingacci, Laura, Beccano-Kelly, Dayne A. ORCID: https://orcid.org/0000-0003-3592-8354, Di Filippo, Massimiliano, Tozzi, Alessandro and Calabresi, Paolo
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From synaptic dysfunction to neuroprotective strategies in genetic Parkinson’s disease: lessons from LRRK2.
Frontiers in Cellular Neuroscience
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Überbacher, Christa, Obergasteiger, Julia, Volta, Mattia, Venezia, Serena, Müller, Stefan, Pesce, Isabella, Pizzi, Sara, Lamonaca, Giulia, Picard, Anne, Cattelan, Giada, Malpeli, Giorgio, Zoli, Michele, Beccano-Kelly, Dayne ORCID: https://orcid.org/0000-0003-3592-8354, Flynn, Rowan, Wade-Martins, Richard, Pramstaller, Peter P, Hicks, Andrew A, Cowley, Sally A and Corti, Corrado
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Application of CRISPR/Cas9 editing and digital droplet PCR in human iPSCs to generate novel knock-in reporter lines to visualize dopaminergic neurons.
Stem Cell Research
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Cav2.3 channels contribute to dopaminergic neuron loss in a model of Parkinson’s disease.
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Chronic and acute LRRK2 silencing has no long-term behavioral effects, whereas wild-type and mutant LRRK2 overexpression induce motor and cognitive deficits and altered regulation of dopamine release.
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Retromer-dependent neurotransmitter receptor trafficking to synapses is altered by the Parkinson's disease VPS35 mutation p.D620N.
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LRRK2 overexpression alters glutamatergic presynaptic plasticity, striatal dopamine tone, postsynaptic signal transduction, motor activity and memory.
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