Parkinson’s disease (PD) is a neurodegenerative disorder for which only symptomatic treatments, such as levodopa and dopamine agonists are available. These drugs ameliorate motor symptoms however they could induce adverse side effects. The mechanism that drives the chronic progression of PD remains elusive. Among the proposed underlying pathophysiological mechanisms, aggregation of α-synuclein, neuroinflammation, and oxidative stress, have been credited to contribute to neuronal loss. Thus, to efficiently modify the course of neurodegeneration in PD, an ideal drug should be capable of interfering with α-synuclein aggregation, halting the generation of toxic species, and inhibiting neuroinflammatory processes. Doxycycline (DOX), a wide-spectrum antibiotic that belongs to the group of the tetracyclines has been suggested by our international research team for repurposing in PD, due to the fact that it has anti-inflammatory and antioxidant properties and mitigates the loss of dopaminergic neurons in an animal model of PD. In addition, we showed that DOX inhibit the pathological aggregation of α-synuclein by reshaping toxic oligomeric species towards strains with reduced toxicity, seeding capacity, and propensity to form amyloid fibril and attenuates the production of mitochondrial-derived reactive oxygen species. During my talk, I will provide strong evidence that doxycycline treatment may be an effective strategy against PD and other synucleinopathies.