Gibbs Lab
Biology Department at New York University
Biology Department at New York University
We explore the intricate mechanisms that sustain neuronal health, with a special focus on mitochondrial function and the critical process of mRNA transport in neurons. Our research aims to understand how neurons maintain mitochondrial integrity and function, particularly in distant regions of the neuron. This involves the transport of mitochondria, local protein synthesis, and the degradation of damaged components to preserve cell health.
We are also interested in how failures in these processes can lead to neurodegenerative diseases such as Parkinson’s disease. By uncovering how neurons manage to support distal mitochondrial function and repair, we aim to understand how mitochondrial quality control pathways influence neuroprotective and regenerative mechanisms.
Through our research, we strive to provide deeper insights into how mitochondrial homeostasis influences neuronal resilience, aging, and recovery, ultimately deepening our knowledge into the interconnection of mitochondria with neural survival pathways.
We are interested in deciphering which mechanisms contribute to the tethering of mRNA to the mitochondria, which has been shown to be a translational hub. Additionally, we are exploring what cellular conditions/ stressors influence mRNA transport on the mitochondria to better understand how local translation directly impacts neuronal survival in disease-related conditions.
We will explore how cell specific differences in mRNA transport and mitochondrial homeostasis contributes to the mechanisms behind selective neuronal vulnerability in respect to aging. Focus on understanding how different neuronal subtypes have distinct mitochondrial needs, dynamics and response to stress will provide crucial insights into the factors that introduce vulnerability in neurodegenerative diseases.
A key perspective that we are investigating is the role of local protein synthesis during initial growth and regeneration periods. We are exploring how delivery of nuclear-encoded mRNA via axonal mitochondria influences regenerative capacity following axonal injury. Additionally, we are interested in how these mechanisms contribute to the progression of neurodegenerative diseases and mitochondrial stress models.