Chiara Invernizzi

c.invernizzi14@campus.unimib.it

ORCID ID: 0009-0003-7506-9344

Curriculum: Experimental Neuroscience

Tutor: Professor Guido Cavaletti

Supervisor: Dr Paola Alberti

Workplace: Università degli Studi di Milano-Bicocca, via Cadore 48, 20900 Monza, Italy
Abroad period: Atlanta, Georgia (Jan-Apr 2025)

Chiara Invernizzi is an experienced PhD student and research fellow at the Università degli Studi di Milano-Bicocca, specializing in the role of ion channels in peripheral neuropathies. Her research, supervised by Dr. Paola Alberti, investigates the sodium-calcium exchanger’s (NCX) involvement in axonal damage. She holds a Master’s degree in Biology applied to biomedical research and a Bachelor’s degree in Biological Sciences. Chiara’s technical expertise includes immunofluorescence, confocal microscopy, primary neuronal cultures, and in vivo administrations. She completed an Erasmus traineeship in Prof. Tiago Outeiro’s Neurodegeneration Lab at the University of Göttingen and she spent some months at Georgia Institute of Technology in Atlanta, GA, USA to perform some experiments for the PhD project. Proficient in English, she excels in team building, time management, and effective communication.

PhD research project
Sodium-calcium exchanger (NCX) and ion channels: pivotal elements leading to axonal damage in peripheral nerves?

Aims:

Investigate the role of specific ion channels, particularly the sodium-calcium exchanger (NCX), in chemotherapy-induced peripheral neuropathies, focusing on reverse mode activation causing intracellular calcium accumulation and axonal damage.
– Evaluate various biomarkers for axonal damage, as there is currently no gold standard for detection.


Background:

Peripheral neuropathies affect 2-3% of the global population, leading to numbness, neuropathic pain, and impaired balance, significantly reducing the quality of life. The underlying pathological mechanisms are not fully understood, but sodium voltage-operated channels (NaV) are implicated, with some studies identifying gain-of-function mutations causing axonal damage. The interplay between NaV and NCX, particularly in the context of ion imbalances, may lead to calcium overload and subsequent axonal damage through toxic events like calpain and phospholipase activation, and synaptic dysfunction.
The oxaliplatin (OHP)-induced peripheral neurotoxicity (OIPN) model will be used to study these mechanisms. OIPN presents in two syndromes: chronic, marked by persistent axonal damage, and acute, characterized by transient symptoms such as cold-induced paraesthesia and cramps, similar to genetic NaV channelopathies. This research aims to elucidate the roles of NaV and NCX in peripheral neuropathies and identify reliable biomarkers for detecting axonal damage.

Further info

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Chiara Invernizzi