Autophagy, together with the ubiquitin proteasome system, is an intracellular degradation pathway that contributes to the destruction and recycling of altered constituents in the cell. However only autophagy can remove large aggregates and whole damaged organelles, which accumulate in the major neurodegenerative diseases. Therefore, bursting autophagy activity in the brain could help ameliorating the removal of toxic constituents that occurs during physiological and pathological aging.
As most cells in the body, neurons and glia possess a primary cilium in their surface, a microtubule based organelle that is required for cell migration during development, and that acts as a major sensory antenna transducing extracellular signals into the intracellular milieu. Neuronal and glial primary cilia respond to neurotrophins, growth factors, hormones and other signals that are able to modulate intracellular events such as autophagy. However, despite the increasing identification of signaling pathways that require the primary cilium for their effector mechanisms, the cellular mechanisms that govern these pathways are poorly understood in the adult brain.
Our lab is aimed to understand the ciliary signaling pathways that modulate autophagy in neurons and glia, as well as the alterations in these ciliary signaling mechanisms that could contribute to the accumulation of toxic components in the brain. Ultimately, the understanding of brain ciliary signaling pathways could contribute to developing new tools to burst autophagy function in neurodegenerative diseases.
Life & Medical Sciences
- Biosciences & Health
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