Janssen Research & Development, LLC announced today the publication of an article that reviews the growing evidence that impaired mitochondrial function may play a major role in mood and psychotic disorders. The review discusses recent data from a wide array of human and animal studies that strongly support the theory that impaired mitochondrial function might disrupt neural plasticity pathways and reduce cellular resilience. These changes may, in turn, promote the development or progression of mood disorders such as major depression and bipolar disorder (BPD), as well as other psychiatric disorders for which the evidence is more limited, such as autism and schizophrenia. The article, "Impaired mitochondrial function in psychiatric disorders," is published in the May 2012 issue of NATURE REVIEWS/Neuroscience.
The studies discussed in the review highlight the high incidence of psychiatric illness in many diseases where mitochondrial dysfunction or genetic mitochondrial defects are present. Further, the studies suggest that 'healthy' mitochondrial function may be a key regulator of synaptic strength and cellular resilience in neuronal circuits that mediate complex, high-order brain functions such as cognition, affect, perception, and behavior.
"Unlocking the mysteries of brain function is fundamental to addressing the health and wellness of people who suffer from disorders like depression, bipolar disorder, and autism," said Husseini K. Manji, M.D., Global Therapeutic Area Head for Neuroscience, Janssen Research & Development, LLC and lead author of the review. "In elucidating the role of mitochondrial function in the development and progression of these diseases, we are uncovering potential new avenues for their treatment. Our goal is to advance additional research and the development of new and novel therapeutics for these complex disorders."
To help advance the development of such novel therapies, the authors call for increased research into mitochondrial dysfunction, and stress the need for new strategies in the development of truly novel treatments for highly disabling psychiatric illnesses. In particular, they advocate the testing of compounds with improved central nervous system (CNS) penetration, as well as compounds other than simple antioxidants.
Because mitochondria play a broad and fundamental role in cellular processes, the development of novel therapeutics that specifically target mitochondria might be considered particularly challenging, given their potential CNS-specific effects. Thus, the authors also propose an innovative and potentially more efficient approach to drug development: one in which the smallest common denominator is targeted as the treatment; subsequent efforts would be aimed at scaling up treatments to yield benefits that are more broadly applicable across a range of diseases sharing underlying origins. In the context of the review, disorders for which either the primary defect occurs in the mitochondria or where there is strong evidence that mitochondria play a key role in disease pathology would represent the most likely targets for treatment success. If successful, this strategy could potentially benefit an entire family of disorders associated with mitochondrial dysfunction in an efficient, cost-effective way.
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