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Anita Bechtholt, PhD

Fellow_McLean_Headshot_Bechtholt_Anita_2008

Anita Bechtholt, PhD

Organization

McLean Hospital

Program

McLean Hospital Mental Health Research Scholars

Year

2008 - 2009

For nearly 30 years, the funding provided by the Rappaport Foundation to physicians and researchers has allowed brilliance to flourish and breakthroughs to triumph in the areas of neurologic diseases and mental illness.

The Rappaport Foundation is allowing me to reach my aspirations of becoming an independent investigator, which will help me achieve my ultimate goal of reducing human suffering. Major depression is an extremely debilitating psychiatric disorder that affects more than 121 million people worldwide. The World Health Organization ranks depression as the leading cause of disability and among the greatest contributors to human suffering. Suicide rates may be as high as 15% among those diagnosed and estimates of resistance to currently available treatments range between 35 and 70%. Despite these startling statistics, little progress has been made over recent years in understanding the causes of depression or in identifying more effective treatments. This lack of increased understanding is likely derived from the fact that the majority of current treatments were discovered by chance more than 20 years ago without any basis in the possible causes of the disease.

More recently it has been established that patients with major depression exhibit over-activation of specific cortical brain areas and a lack of cortical glial cells, which serve to support neurons and modulate the communication between neural cells. The major goal my work is to recapitulate these abnormalities by preventing glial cells from processing the excitatory neurotransmitter glutamate. The hypothesis guiding this work is that decreased glial trafficking of glutamate can precipitate deleterious effects that underlie the pathophysiology of depression. Through the support of the Rappaport Foundation I have been able to demonstrate that a lack of glial cell function is sufficient to induce a depressive-like state, suggesting that a lack of glial cells in the depressed brain may indeed have a causal role in depression. In the future I hope to target the function of glial cells to develop new treatment ideas that, unlike the currently available treatments, are based in what we know is different about the depressed brain.

My major interest in this work is from a perspective of compassion. I find it tragic that so many people suffer from this painful disorder that is not well treated or understood. The support of the Rappaport Foundation has allowed me to work on improving this situation by making important contributions to the depression field that will certainly improve treatment over time. These discoveries also have important role in the advancement of my scientific career. Since beginning my Rappaport Foundation Fellowship I have been able to collect exciting data will be the basis for additional grant applications and publications, but have also been promoted and invited to influential scientific meetings. Taken together, the Rappaport Foundation is allowing me to reach my aspirations of becoming independent investigator, which will help me achieve my ultimate goal of reducing human suffering.