Background: Parkinson’s disease (PD) is a progressive neurodegenerative disorder where the loss of dopaminergic neurons in the substantia nigra and the presence of Lewy bodies in surviving neurons are primary histopathological hallmarks. Recent evidence points to mitochondrial dysfunction as a common upstream event in PD etiopathology. Objective: In this overview, we will discuss some of our findings that provide support for the mitochondrial cascade hypothesis, whereas mitochondrial deficits trigger PD pathology through alterations in microtubule integrity and macroautophagy. Methods: Using, as a PD model, cells that have PD patients’ mitochondrial DNA, cells without mitochondrial DNA and MPP+-treated cells, we showed that mitochondrial metabolism alteration may underlie changes in the microtubular net and in the autophagic-lysosomal pathway. Conclusions: Finally, we will endow a potential new therapeutic target for PD pathology.
