In a case of hepatocerebral disease of Inose type the astrocytes, corresponding to Alzheimer type II glia, had swollen cytoplasm containing glycogen granules and focal aggregates of lipofuscin granules. Their nuclei contained bodies of simple and of complex types as well as conglomerates of glycogen granules without any capsules. The nuclear bodies of simple type were also observed in the nuclei of endothelial cells. It is concluded that these changes in the appearance of Alzheimer type II glia suggest reactive and defensive changes in the brain against ammonium ions, rather than being merely degenerative in nature.
Long-term (6 months) administration of 25 mg/kg body weight/day chlorpromazine (CPZ) to rats resulted in remarkable inhibition of normal increase with age of osmiophilic lipid droplets (OLD) in the pineal gland, and atrophy of pinealocytes. The breeding conditions such as illumination, humidity, and room temperature were strictly controlled. Hence, these changes were ascribed solely to the effects of the drug. OLD are considered as an indicator of physiological activity of the gland. In view of the possible functional relations of this organ to endocrine or autonomic nervous activity, our finding may give a clue to the clarification of the possible cause of some side-effects of the drug.
Lesions in the CNS induced by 6-aminonicotinamide (6-AN) presented a spongy state of the gray matter and neuronal chromatolysis. With aging of the experimental animals the lesions extended from the phylogenetically early developed structures to those developed later, i.e., from spinal gray matter, dentate nuclei, and brain stem nuclei through limbic structures and striatum to the cerebral cortex. Changes of the neurons were more prominent with aging. Lesions in the CNS of rats at the age, corresponding to the involutional period in the human, were similar to those of Creutzfeldt-Jakob disease (C-J) disease) in the presenile age. In recent years, the resemblance between C-J disease and pellagra encephalopathy had been noted by several authors, and they resemble the lesions caused by 6-AN, an antimetabolite of nicotinamide used in our experiment. This evidence, therefore, has led to the hypothesis that dysfunction of NAD(H)- or NADP(H)-dependent enzymes in the CNS of the aged, even if not the primary cause, may be one possible pathogenetic factor of C-J disease.
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