- Autophagy-apoptosis cross talk
- Cellular antioxidants
- Neurobiology of diseases
- Neuron-glial interaction
- Oxidative stress
- Protein degradation systems
- Stem cell biology
- Role of oxidative stress in pathophysiology of neurodegenerative disease
- Neuroprotection strategies for treatment of spinal cord injury
- Examination of nuclear events in neurodegenerative diseases
- Role of thioredoxin system in health and disease
- Aging and neurodegeneration
- Neural stem cells biology and their application for human diseases
- Oxidative stress
- Regulated cell death systems
- Thioredoxin system
Dr. Eftekhar Eftekharpour’s laboratory is focused on examination of molecular events in neuronal health and disease. The lab aims to understand how neurons maintain their complex structure and function.
Neurons rely on high levels of oxidative phosphorylative respiration for energy production and therefore are exposed to high levels of reactive oxygen species (ROS). This increases the possibility of oxidative damage of cellular proteins.
Neurons have developed efficient protein degradation systems to recycle the old and damaged proteins by their proteasome and in their lysosomes. Deficiency of these systems in aging and in neurodegeneration diseases result in accumulation of damaged and undigested proteins, causing neuronal death. Alzheimer’s disease (AD) is the most common form of these diseases and is identified by accumulation of Amyloid plaques and formation of neurofibrillary tangles.
The lab focuses on understanding why these events occur, and the thioredoxin system, a major antioxidant system, which is known to decrease in AD brain.
Dr. Eftekharpour’s research has shown that thioredoxin deficiency can unleash a series of events resulting in alteration of lysosomes and in neuronal nuclei.
Information driven from this basic research has led us to formulate novel therapeutic approaches for targeting neuronal cell death after spinal cord injury and AD.
Another aspect of Dr. Eftekharpour’s research in our group investigates the involvement of cellular redox status in neural stem cells proliferation, differentiation, and death.
Using patient derived neurons to model neurodegenerative diseases, we aim to enhance our understanding of the disease and to use them for drug discovery approaches.