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OUR VISION

We investigate how neural circuitry is structurally and functionally affected in ALS or TBI by cutting-edge viral tools, tracing strategies, chemiogenetic systems and animal models; we extend this expertise to the analysis of neural and synaptic structures in other neurological conditions, building on our know-how and capabilities in spinal cord research. The Roselli group acquires and develops the technological means to investigate pathomechanisms in vivo with the highest level of spatio-temporal control and biological fidelity, using highly-multiplexed approaches to reconstruct complex events (from signaling to network remodeling).

Amyotrophic Lateral Sclerosis

Synaptic dysfunction in Motoneuron Disease

We investigate how disruption of synaptic inputs may contribute to determine motoneuron vulnerability and to drive neurodegeneration in Amyotrophic Lateral Sclerosis; we exploit multiplexed chemogenetics and several mouse models and human pathological samples.

Innovative therapeutic modalities for Motoneuron Disease

We study new neuromodulators that allow motoneuron-specific therapeutic interventions with small molecules; in a parallel project, we develop new AAV vectors for experimental manipulation of Motoneurons and for gene therapy.

Vascular biology of Motoneuron Disease

We use multiplexed chemogenetics to untangle the vascular and neuroinflammatory contributions to motoneuron degeneration in multiple ALS mouse models.

Large-scale neuronal circuit structure in Motoneuron Disease

We use viral vector tracing and advanced approaches in neuroinformatics and high-resolution optical imaging to observe the large-scale changes in neuronal circuits occurring before onset and during progression of ALS.

Hypothalamus in motoneuron disease

 

 

we participate in clinical and experimental research with the goal to identify and modulate the mechanisms responsible for hypermetabolism in ALS.

Hypothalamus in motoneuron disease

We participate in clinical and experimental research with the goal to identify and modulate the mechanisms responsible for hypermetabolism in ALS.

Traumatic Brain Injury

Neuronal activity in TBI vulnerability 

We study how the activity of cortical microcircuits determine neuronal vulnerability in TBI and how neurons control microglia and neuroinflammatory responses in TBI.

Large-scale signaling in TBI

We study the large-scale architecture of signaling events set in motion by TBI in neurons, microglia and other CNS cell types, with the ultimate goal to repurpose FDA-approved drugs for acute TBI treatment.

Non-coding RNA in TBI

We investivate the role of a number of non-coding RNA in regulating the acute response and the regeneration phase of TBI.

Cytokines-driven synaptic events 

We study how TBI-induced cytokines modulate composition and turnover of synapses from early to chronic stages.

Ethanol and TBI

 

We study the interplay of ethanol intoxication and TBI pathogenic cascades, aiming at determining if ethanol is ultimately beneficial or detrimental in TBI.

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