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Abstract #0597

Tissue Specific Changes in Brain Phosphodiesters in Late Life Major Depression

David G. Harper1,2, J. Eric Jensen, 2,3, Caitlin Ravichandran, 2,4, E. Yusuf Sivrioglu5, Daniel Iosifescu6,7, Perry Renshaw8, Brent Forester, 29

1Geriatric Psychiatry, McLean Hospital, Belmont, MA, United States; 2Psychiatry, Harvard Medical School, Belmont, MA, United States; 3Neuroimaging Center, McLean Hospital, Belmont, MA, United States; 4Laboratory for Psychiatric Biostatistics, McLean Hospital, Belmont, MA, United States; 5Psychiatry, Uludag University, Bursa, Turkey; 6Psychiatry, Massachusetts General Hospital, Boston, MA, United States; 7Psychiatry, Harvard Medical School, Boston, MA, United States; 8Psychiatry, University of Utah, Salt Lake City, UT, United States; 9Geriatric Psychiatry, Mclean Hospital, Belmont, MA, United States


Biological membranes serve numerous, essential cellular functions. MRI findings in late life depression include increased white matter hyperintensities and reduced fractional anisotropy as measured by diffusion tensor imaging suggesting that membrane integrity, especially in white matter, may be compromised. Phosphatidylethanolamine, in the inner mitochondrial membrane, serves an essential function and is synthesized via a unique pathway not involving phosphoethanolamine. We hypothesized that glycerophosphocholine (GPCho) and glycerophosphoethanolamine (GPEtn), particularly in white matter, will be increased in late-life depression, and we hypothesized that GPEtn will be altered fundamentally differently than GPCho due to the additional pathway of the inner mitochondrial membrane and that GPEtn would therefore show changes in gray matter.

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