CORTICAL SYNAPTIC CHANGES AND GLIOSIS IN NORMAL AGING, ALZHEIMERS-DISEASE AND FRONTAL-LOBE DEGENERATION

The most important new development during recent years in the field of degenerative dementia concerns synaptic pathology. So far it has been investigated in some regions and same cortical laminae in Alzheimer's disease (AD). The present communication is a more comprehensive study of all laminae in four different regions, the prefrontal, parietal, i nferior temporal and posterior cingulate cortex. Against the backgroun d of normal aging, AD was compared with another degenerative disorder, frontal lobe degeneration of non-Alzheimer type (FLD). The synapse de nsity was measured using synaptophysin as a marker. Astrocytes were al so counted in the molecular layer. In normals, the cortex showed succe ssively lower synaptic density from layer I to layer VI and relatively lowest density in the prefrontal cortex and a general decline with in creasing age. A 46-49% decrease in synaptic density was found in all l aminae in all regions of AD brains, a finding different from that in F LD, The number of astrocytes increased significantly in the prefrontal cortex both in AD and FLD but parietally only in AD, These results co ntribute to the understanding of normal synaptic organization of corte x, demonstrate the laminar and regional distribution of synaptic loss in AD and underscore the difference between AD and FLD, The gliosis ap pears to be secondary to the neurodegenerative changes. Synaptic loss is likely to be a common pathogenetic feature of neurodegenerative dis orders and a likely cause of clinical symptoms and regional metabolic decrements in dementia.