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By Sid Gilman

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Extra resources for Neurobiology of Disease

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AGAT deficiency Creatine deficiency syndromes (CDSs) are a novel group of inborn errors of creatine metabolism including the biosynthetic disorders arginine:glycine amidinotransferase deficiency (AGAT; MIM 602360) and guanidinoacetate methyltransferase deficiency (GAMT; MIM 601240), and a defect of the creatine transporter, SLC6A8 deficiency (SLC6A8; MIM 300036). In all these disorders, the common clinical hallmark is mental retardation, expressive speech delay, and epilepsy; the common biochemical hallmark is cerebral creatine deficiency as detected by proton magnetic resonance spectroscopy (H-MRS).

Thus, in the sensorineural deafness and pigmentary retinopathy, the lesion appears to reside in specialized sensory neurons [3]. The fifth lesion is restricted to the neurons of the dorsal nuclei of Clarke and the lateral cuneate nuclei, secondorder sensory neurons, which demonstrate striated perikarya because of the accumulation or storage of lamellar and lipid profiles of abnormal cholesterol esters containing VLCFA. This is accompanied by lamellae and lipid clefts within neighboring axonal spheroids virtually identical to those seen in infantile neuroaxonal dystrophy.

Neurol. ) inferior olivary and dentate nuclei are present. These fetal lesions confirm the prediction that the insult (presumably metabolic) causing the neocortical migration defect is operating throughout the entire neocortical neuronal migratory period [14]. Immunohistochemical deficiencies of the cell adhesion molecule L1 and doublecortin have been reported in fetal Zellweger brains [1]. Based on the human postmortem studies of ZS, particularly of the fetuses at risk, we have proposed Pathogenetic insights and hypotheses can arise from human morphological and biochemical studies, but true cause-and-effect relationships cannot be established through this method of scientific investigation.

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