Novel mechanistic insights into the role of mitochondria in Parkinson’s disease

Parkinson’s disease (PD) is a common neurodegenerative disorder characterized the selective loss of dopamine (DA) neurons in the Substantia Nigra of the midbrain and severe DA depletion in the striatum, which manifest as motor impairment.More than ten million people worldwide live with PD and yet, there is currently no cure for this devastating condition.

Improving our understanding of PD pathophysiology is therefore crucial to identify novel therapeutic strategies.Growing evidence indicates that mitochondrial dysfunction is heavily implicated in PD, although the underlying molecular mechanisms remain unclear. The aim of this proposal is to investigate how mitochondrial fitness is involved in the maintenance of DA neurons.

In the next four year, my research team will explore in depth (i) CHCHD2 as a novel PD-gene encoding a highly conserved mitochondrial protein of unknown function; (ii) the impact of mitochondrial dysfunction on DA neurons gene expression; (iii) the importance of mitochondria-driven neuroinflammation in PD.

At Karolinska Institutet, my research group will work in close collaboration with world-class experts in the field and employ genetic, molecular and omics approaches in order to dissect the molecular events driving DA degeneration.

Our in vitro and in vivo work will provide unprecedented mechanistic insights into the role of mitochondria in PD onset and progression and set the ground for innovative and more targeted therapies.