By Kunihiko Suzuki, Kinuko Suzuki (auth.), Gerald E. Gaull (eds.)
The progress of neurochemistry, molecular biology, and biochemical genetics has ended in a burgeoning of latest details correct to the pathogenesis of mind disorder. This explosion of interesting new info is crying out for collation and significant synthesis. In its totality, it defies systematic summa tion, and, in fact, not anyone writer can cope. hence invites for contributions got to varied specialists in parts that are below lively research, of present neurological curiosity, and pregnant. even though this undertaking is comparatively entire, through dint of measurement, different issues could have been incorporated; the choice was once exclusively my accountability. i feel systematic summation a digital impossibility-indeed, infrequently well worth the attempt. The try and gather the entire sections eager about a wide treatise with a number of authors necessarily leads to untoward delays as a result distinction within the price at which quite a few authors paintings. consequently, the subsequent process has been followed: a number of small volumes and a comparatively versatile structure, with e-book so as of receipt and once sufficient chapters are assembled to make book sensible and low-cost. during this approach, the time lag among the information and their emergence in print is the shortest.
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Additional resources for Biology of Brain Dysfunction: Volume 2
Two types of abnormal inclusions are found in globoid cells. The first, more common type of the inclusion is a moderately electron-dense, straight or curved hollow tubular structure with irregularly crystalloid cross sections. (144) The second type of abnormal inclusion Fig. 5. Light microscopic appearance of white matter in globoid cell leukodystrophy. The numerous abnormal globoid cells stain PAS positive. The remainder of white matter is replaced by severe reactive gliosis, and the myelin sheath is essentially absent.
11). Excess lactosylceramide was not inhibitory, and mixing experiments excluded the presence of inhibitors in the pathological tissue. The same deficiency was demonstrated in cultured fibroblasts of the patient. In this instance, a 50% reduction of tJ-glucosidase was also observed-an interesting finding in relation to the increased glucocerebroside in the liver, 35 Disorders of Sphingolipid Metabolism t ceramide-glucose-galactose (Iactosylceramide) loc""ylcernm;de goloct",ldaH ceramide-glucose + galactose (g lucocerebroside) Fig.
Hepatosplenomegaly was present, and there were abnormal mononuclear storage cells with foamy cytoplasm in the bone marrow. Serum acid phosphatase was elevated. The patient's neurological signs gradually worsened, and she died at age 4. The parents were not consanguineous, and there was no family history of neurological disorders. There is, therefore, no clue as to the genetic nature of the disease except for the partial reduction of lactosylceramide galactosidase in skin fibroblasts of both parents, as discussed below, which suggests the autosomal recessive mode of inheritance.
Biology of Brain Dysfunction: Volume 2 by Kunihiko Suzuki, Kinuko Suzuki (auth.), Gerald E. Gaull (eds.)