Davide Trotti

A caspase-3-cleaved fragment of the glial glutamate transporter EAAT2 is sumoylated and targeted to promyelocytic leukemia nuclear bodies in mutant SOD1-linked amyotrophic lateral sclerosis.

Nordihydroguaiaretic acid increases glutamate uptake in vitro and in vivo: therapeutic implications for amyotrophic lateral sclerosis.

Glutamate transporters and the excitotoxic path to motor neuron degeneration in amyotrophic lateral sclerosis.

ALS-linked mutant SOD1 damages mitochondria by promoting conformational changes in Bcl-2.

Voltage-dependent inwardly rectifying potassium conductance in the outer membrane of neuronal mitochondria.

Motor neuron impairment mediated by a sumoylated fragment of the glial glutamate transporter EAAT2.

An over-oxidized form of superoxide dismutase found in sporadic amyotrophic lateral sclerosis with bulbar onset shares a toxic mechanism with mutant SOD1.

Selective increase of two ABC drug efflux transporters at the blood-spinal cord barrier suggests induced pharmacoresistance in ALS.

Small peptides against the mutant SOD1/Bcl-2 toxic mitochondrial complex restore mitochondrial function and cell viability in mutant SOD1-mediated ALS.

Sumoylation of critical proteins in amyotrophic lateral sclerosis: emerging pathways of pathogenesis.

Role of mitochondria in mutant SOD1 linked amyotrophic lateral sclerosis.

ABC transporter-driven pharmacoresistance in Amyotrophic Lateral Sclerosis.

Antisense proline-arginine RAN dipeptides linked to C9ORF72-ALS/FTD form toxic nuclear aggregates that initiate in vitro and in vivo neuronal death.

Inhibiting drug efflux transporters improves efficacy of ALS therapeutics.

Regulation of ABC efflux transporters at blood-brain barrier in health and neurological disorders.

Astrocytes drive upregulation of the multidrug resistance transporter ABCB1 (P-Glycoprotein) in endothelial cells of the blood-brain barrier in mutant superoxide dismutase 1-linked amyotrophic lateral sclerosis.

Pathogenic determinants and mechanisms of ALS/FTD linked to hexanucleotide repeat expansions in the C9orf72 gene.

Cell-to-Cell Transmission of Dipeptide Repeat Proteins Linked to C9orf72-ALS/FTD.

Mutation of the caspase-3 cleavage site in the astroglial glutamate transporter EAAT2 delays disease progression and extends lifespan in the SOD1-G93A mouse model of ALS.

Blood-Brain Barrier Driven Pharmacoresistance in Amyotrophic Lateral Sclerosis and Challenges for Effective Drug Therapies.

EAAT2 and the Molecular Signature of Amyotrophic Lateral Sclerosis.

Astrocytes expressing ALS-linked mutant FUS induce motor neuron death through release of tumor necrosis factor-alpha.

Haploinsufficiency leads to neurodegeneration in C9ORF72 ALS/FTD human induced motor neurons.

miR126-5p Downregulation Facilitates Axon Degeneration and NMJ Disruption via a Non-Cell-Autonomous Mechanism in ALS.

Repeat-associated non-AUG translation in C9orf72-ALS/FTD is driven by neuronal excitation and stress.

Excess glutamate secreted from astrocytes drives upregulation of P-glycoprotein in endothelial cells in amyotrophic lateral sclerosis.

Synaptic dysfunction induced by glycine-alanine dipeptides in C9orf72-ALS/FTD is rescued by SV2 replenishment.

Proteostatic imbalance and protein spreading in amyotrophic lateral sclerosis.