A pathological hallmark of many age-associated neurodegenerative diseases is the presence of misfolded protein aggregates, indicating disturbances in proteostasis. Protein aggregates in the cell are cleared by autophagy, a cellular pathway known to be impaired in several neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, Huntington's disease and amyotrophic lateral sclerosis. However, the precise mechanism, which leads to autophagosomal malfunction in neurons and its relationship to protein aggregations and neuronal death remains unresolved. It is currently not known whether the increase in autophagosomes observed in the degenerating neurons plays a protective role or instead contributes to the pathology of the neurodegeneration. 

Natalia Kononenko’s lab integrates molecular, genetic and cell biology approaches with live cell imaging, state-of-the-art superresolution microscopy and in-vivo neuroanatomy techniques (including track-tracing techniques and 3D neuronal reconstructions) to understand the role of membrane trafficking and autophagy in the pathogenesis of age-dependent neurodegenerative diseases.