Altered expression of NCAM in hippocampus and cortex may underlie memory and learning deficits in rats with streptozotocin-induced diabetes mellitus.

Neurological and structural changes are paralleled by cognitive deficits in diabetes mellitus. The present study was designed to evaluate the expression of neural cell adhesion molecules (NCAM) in the hippocampus, cortex and cerebellum and to examine cognitive functions in diabetic rats. Diabetes was induced in male albino rats via intraperitoneal streptozotocin injection.

Altered glial fibrillary acidic protein content and its degradation in the hippocampus, cortex and cerebellum of rats exposed to constant light: reversal by melatonin.

Reactive astrocytosis is a well-known phenomenon that occurs rapidly after physical or metabolic injury to the brain. One of the important events during astrocyte differentiation is the increased expression of glial fibrillary acidic protein (GFAP), a member of the family of intermediate filament structural proteins. Free radicals are neurotoxic and free radical scavengers have been shown to protect the brain against neurotoxic damage.