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Abnormal cerebral phospholipid metabolism in dyslexia indicated by phosphorus‐31 magnetic resonance spectroscopy
Author(s) -
Richardson Alexandra J.,
Cox I. Jane,
Sargentoni Janet,
Puri Basant K.
Publication year - 1997
Publication title -
nmr in biomedicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.278
H-Index - 114
eISSN - 1099-1492
pISSN - 0952-3480
DOI - 10.1002/(sici)1099-1492(199710)10:7<309::aid-nbm484>3.0.co;2-0
Subject(s) - phospholipid , dyslexia , chemistry , membrane , metabolism , phosphomonoesters , biochemistry , nuclear magnetic resonance spectroscopy , phosphorus , endocrinology , medicine , nuclear magnetic resonance , biology , stereochemistry , enzyme , organic chemistry , physics , reading (process) , political science , law , inorganic phosphate
It has recently been suggested that many of the features of dyslexia may be explicable in terms of an abnormality of membrane phospholipid metabolism. To investigate this we studied 12 dyslexic and 10 non‐dyslexic adults using in vivo cerebral phosphorus‐31 magnetic resonance spectroscopy ( 31 P MRS), as the phosphomonoester (PME) and phosphodiester (PDE) peaks include indices of membrane phospholipid turnover. Spectral localization was achieved using four‐dimensional chemical shift imaging methods. The PME peak area was significantly elevated in the dyslexic group, as evidenced by higher ratios of PME/total phosphorus ( F =9.5, p <0.006), PME/NTP ( F =17.5, p <0.001) and PME/PDE ( F =6.9, p <0.02). No other spectral measurements differed significantly between the groups. These findings are consistent with the hypothesis that membrane phospholipid metabolism is abnormal in dyslexia. The PME peak is multicomponent, but predominantly consists of phosphoethanolamine (PE) and phosphocholine (PC), which are precursors of membrane phospholipids. Our finding of raised PME in dyslexia could therefore reflect reduced incorporation of phospholipids into cell membranes, although definitive interpretation must await further evidence. © 1997 John Wiley & Sons, Ltd.