Structural changes in the normally aging cerebral cortex of primates.
During normal aging humans exhibit some cognitive decline, but it is difficult to determine the underlying causes of this decline, because information about cognitive status is rarely available and preservation of the brain is usually inadequate for detailed cytological examination. One solution to this problem is to use a nonhuman primate model, such as the rhesus monkey, which exhibits age-related cognitive decline similar to humans, and can be cognitively tested before the brains are preserved for detailed examination. It is now known that cognitive decline in human and nonhuman primates is not due to loss of cortical neurons and there is no correlation between the frequency of senile plaques and cognitive status. Indeed apart from layer 1, neurons of cerebral cortex show few signs of aging, although there may be some loss of synapses throughout cortex. In contrast, both microglia and astrocytes come to contain phagocytosed material, but its origin is unknown. There is also loss of white matter, which is accompanied by some breakdown of myelin sheaths and alterations in oligodendrocytes. It is suggested that the myelin changes alter conduction velocities along axons. This would alter timing in neuronal circuits, contributing to cognitive decline.
Peters
Alan
A
Department of Anatomy and Neurobiology, Boston University School of Medicine, 715 Albany Street, Boston, MA 02118-2526, USA. apeters@cajal-1.bu.edu
D000375:Aging / Q000473:pathology* / Q000502:physiology; D000818:Animals; D002540:Cerebral Cortex / Q000473:pathology* / Q000502:physiology / Q000648:ultrastructure; D003712:Dendrites / Q000473:pathology* / Q000648:ultrastructure; D006801:Humans; D009413:Nerve Fibers, Myelinated / Q000473:pathology* / Q000648:ultrastructure; D009431:Neural Conduction / Q000502:physiology; D009457:Neuroglia / Q000473:pathology* / Q000648:ultrastructure; D011323:Primates / Q000033:anatomy & histology* / Q000502:physiology