Marta Lipinski, PhD

Function and mechanisms of Autophagy in acute CNS injury and age-related neurodegeneration

Autophagy is a catabolic process mediating the turnover of bulk cytoplasmic constituents including organelles and protein aggregates in a lysosome-dependent manner (Figure 1). It is necessary for cellular homeostasis and protects organisms from a variety of diseases, including neurodegeneration and aging. My lab uses a combination of in vivo transgenic mouse models and in vitro cell-based models to investigate the function and mechanisms of autophagy and its perturbation in CNS disease. Our interests include both acute CNS injury due to traumatic brain injury (TBI) and spinal cord injury (SCI) and chronic age-related neurodegeneration in Parkinson’s disease (PD). We are also investigating a potential role for autopahgy in liking history of TBI to development of neurodegeneration and demantia later in life. Our long-term goal is to define novel target molecules and pathways for safe and effective modulation of autophagy as a treatment against neurodegeneration induced by both acute (trauma) and chronic (neurodegenerative diseases) causes.

Figure 1. During autophagy cytoplasmic cargo including proteins, protein aggregates and organelles are sequestered into double-membrane vesicles termed autophagosomes. Autophagosomes then fuse with lysosomes, allowing degradation of their contents by lysosomal proteases. This progress of cargo from sequestration into autophagosomes, to delivery to lysosomes and lysosomal degradation, is termed autophagy flux and is necessary for normal function of autophagy.

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