NAWM in MS has a higher water content and lower myelin water fraction than control white matter. The cause of the myelin water fraction decrease in NAWM could potentially be due to either diffuse edema, inflammation, demyelination or any combination of these features. We present a simple model which suggests that myelin loss is the dominant feature of NAWM pathology.

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Schizophrenia unfolds during the late period of brain maturation, while myelination is still continuing. In the present study, we used MRI and T2 relaxation analysis to measure the myelin water fraction in schizophrenia. In schizophrenia (n ¼ 30) compared with healthy subjects (n ¼ 27), overall white matter showed 12% lower myelin water fraction (P ¼ 0.031), with the most prominent effects on the left genu of the corpus callosum (36% lower, P ¼ 0.002). The left anterior genu was affected in both first-episode (P ¼ 0.035) and chronic patients (P ¼ 0.011). In healthy subjects, myelin water fraction in total white matter and in frontal white matter increased with age, and with years of education, indicating ongoing maturation. In patients with schizophrenia, neither relation was statistically significant. Post-mortem studies of anterior frontal cortex demonstrated less immunoreactivity of two oligodendrocyte-associated proteins in schizophrenia (2 0 ,3 0 -cyclic nucleotide 3'-phosphodiesterase by 33%, P ¼ 0.05; myelin-associated glycoprotein by 27%, P ¼ 0.14). Impaired myelination in schizophrenia could contribute to abnormalities of neural connectivity and persistent functional impairment in the illness. Molecular Psychiatry (2003) 8, 811-820. doi:10.1038/sj.mp.4001337Keywords: myelin-associated glycoprotein; 2 0 ,3 0 -cyclic nucleotide 3 0 -phosphodiesterase; frontal lobe; T2 relaxation; schizophrenia; oligodendrocyte Schizophrenia is one of the most disabling mental disorders, yet the mechanism of illness remains unclear. Abnormalities of dopaminergic neurotransmission contribute to acute exacerbations of illness; 1 however, factors related to illness onset and subsequent disability are less certain. Clinical, neuroimaging, and neuropathological evidence indicates disturbances of early brain development may predispose to schizophrenia. However, the period of brain maturation in adolescence and early adulthood is the window of time during which the illness is first expressed. During this period of maturation, changes in white matter tracts are relatively prominent. [2][3][4][5][6] Diseases of white matter such as leukodystrophies, which may have their onset at this age, frequently present with psychosis as an early feature, 7,8 and multiple sclerosis (MS) may also be associated with psychosis. 9 Abnormalities of white matter in schizophrenia are detected with a range of MRI techniques including image averaging, 10-12 magnetization transfer imaging, 13 diffusion tensor imaging, 14-17 and measurement of transverse relaxation time. [18][19][20][21] The cellular or molecular implications of these findings are not clear. Magnetic resonance spectroscopy (MRS) does detect chemical differences in white matter in schizophrenia. [22][23][24] The observation of lower levels of the neuronspecific maker N-acetylaspartate in white matter suggests abnormalities of axons in schizophrenia.A complementary MRI technique allows analysis of myelin. MRI can detect a signal related to water distribution in tissue. This MRI signal can b...

The ability to measure myelin in vivo has great consequences for furthering our knowledge of normal development, as well as for understanding a wide range of neurological disorders. The following review summarizes the current state of myelin imaging using MR. We consider five MR techniques that have been used to study myelin: 1) conventional MR, 2) MR spectroscopy, 3) diffusion, 4) magnetization transfer, and 5) T2 relaxation. Fundamental studies involving peripheral nerve and MR/histology comparisons have aided in the interpretation and validation of MR data. We highlight a number of important findings related to myelin development, damage, and repair, and we conclude with a critical summary of the current techniques available and their potential to image myelin in vivo.