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Fractional anisotropy of water diffusion in cerebral white matter across the lifespan

P. KochunovabCorresponding Author Informationemail address, D.E. Williamsonacd, J. Lancastera, P. Foxa, J. Cornelld, J. Blangerob, D.C. Glahnae

Received 17 August 2009; received in revised form 15 January 2010; accepted 18 January 2010. published online 01 February 2010.
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Abstract 

Determining the time of peak of cerebral maturation is vital for our understanding of when cerebral maturation ceases and the cerebral degeneration in healthy aging begins. We carefully mapped changes in fractional anisotropy (FA) of water diffusion for eleven major cerebral white matter tracts in a large group (831) of healthy human subjects aged 11–90. FA is a neuroimaging index of micro-structural white matter integrity, sensitive to age-related changes in cerebral myelin levels, measured using diffusion tensor imaging. The average FA values of cerebral white matter (WM) reached peak at the age 32±6 years. FA measurements for all but one major cortical white matter tract (cortico-spinal) reached peaks between 23 and 39 years of age. The maturation rates, prior to age-of-peak were significantly correlated (r=0.74; p=0.01) with the rates of decline, past age-of-peak. Regional analysis of corpus callosum (CC) showed that thinly-myelinated, densely packed fibers in the genu, that connect pre-frontal areas, maturated later and showed higher decline in aging than the more thickly myelinated motor and sensory areas in the body and splenium of CC. Our findings can be summarized as: associative, cerebral WM tracts that reach their peak FA values later in life also show progressively higher age-related decline than earlier maturing motor and sensory tracts. These findings carry multiple and diverse implications for both theoretical studies of the neurobiology of maturation and aging and for the clinical studies of neuropsychiatric disorders.

a Research Imaging Institute, University of Texas Health Science Center at San Antonio, United States

b Southwest Foundation for Biomedical Research, San Antonio, TX, United States

c Department of Psychiatry, University of Texas Health Science Center at San Antonio, TX, United States

d Department of Epidemiology & Biostatistics, University of Texas Health Science Center at San Antonio, TX, United States

e Department of Psychiatry, Yale University & Olin Neuropsychiatric Research Center, CT, United States

Corresponding Author InformationCorresponding author at: University of Texas Health Science Center at San Antonio, Research Imaging Institute, 7703 Floyd Curl Drive, San Antonio, TX 78284, United States. Tel.: +1 210 567 8100; fax: +1 210 567 8152.

PII: S0197-4580(10)00044-8

doi:10.1016/j.neurobiolaging.2010.01.014