Golgi apparatus in Alzheimer’s disease

Abstract

Introduction: Alzheimeŕs disease (AD) is a devastating disorder of the central nervous system, involving progressive cognitive impairment, characterized by profound memory loss, learning inability, behavioral changes, resulting eventually in a vegetative state. The etiopathology of AD, remains still unknown. The implication of β-amyloid, APP, τ protein, the neuronal loss, the synaptic changes, the cytoskeletal alterations, the capillary changes play an important role in the pathogenesis of the disease, without explaining sufficiently the innermost mechanisms. Morphological alterations of the neuronal organelles, mostly concerning the mitochondria, have been described histochemically as well as ultrastructurally. Material and methods: In the present study we attempted to describe the morphological alterations of the Golgi apparatus (GA) in 8 early cases of AD, in post mortem material, promptly fixed and studied in electron microscopy. It is known that GA plays an important role in glycozilation, sulfation and proteolytic processing of protein systems, synthesized in the endoplasmic reticulum of neurons and glial cells. The hyperphosphorylation of τ protein, a phenomenon associated with the pathogenesis of AD, is also related with the pathophysiology of GA. Results: In cases of Alzheimer's disease we observed a marked fragmentation of GA in the perikaryon of polyhedral and pyramidal cells of the hippocampus, the large triangular neurons of the frontal cortex as well as the Purkinje cells of the cerebellum. Conclusion: The fragmentation of Golgi apparatus may be related with the action of β secretase on APP, or it may be associated with the alterations of microtubules, since those cytoskeletal elements play an important role in spacial organization and the integrity of the cisternae of the Golgi apparatus.