Despite intense research efforts aimed at halting or reversing the progression of complex human brain disorders such as Neurodegenerative disease (Alzheimer’s disease, Parkinson’s disease, cerebral stroke), effective therapeutics that significantly modify the course of these diseases have not yet been developed. Therefore, a new paradigm is required for the design of novel therapeutic strategies for treatment of such disorders, especially those that are expected to become more prevalent in aging or aged societies. Mitochondrial electron transport chain (ETC) function has been implicated in the etiology of complex diseases and as a modifier of their clinical course; to date, however, mitochondrial medicine or interventions that would be useful for controlling such disorders remain unavailable.
The blood brain barrier, which composed by endothelial cell, astrocyte and pericyte consider to neurologic disease initiation area by peripheral insults (inflammation, toxic insults). BBB disruption is considered to be a result of oxygen-glucose depletion in ischemic stroke and a symptom of neurodegenerative diseases such as Parkinson’s disease and Alzheimer’s disease. A recent study showed that cyclooxygenase inhibition prevents BBB disruption following ischemic stroke. Although oxidative stress causes BBB disruption and pathogens aggravate BBB dysfunction in neurological diseases, whether mitochondrial modulation can preserve BBB integrity is still unknown. To discover the protective molecule for maintenance of BBB, we will find out the activator of mitochondrial biogenesis and investigate the secretory molecule by mitochondrial dysfunction which affect the surrounding cells (astrocyte, neuron and endothelial interacting factor) with non-cell autonomous mechanism.
Department of Biochemistry
Department of Medical Science
Chungnam National University College of Medicine
Munhwa-ro 266, Jung-gu, Deajeon, Republic of Korea
Tel. 042-580-8363, 8351