Aging and the myelinated fibers in prefrontal cortex and corpus callosum of the monkey.
In the rhesus monkey, the myelin sheaths of nerve fibers in area 46 of prefrontal cortex and in splenium of the corpus callosum show age-related alterations in their structure. The alterations are of four basic types. Most common is splitting of the dense line of myelin sheaths to accommodate electron dense cytoplasm derived from the oligodendroglia. Less common are splits of the intraperiod line to form balloons or blisters that appear to contain fluid, the occurrence of sheaths with redundant myelin, and thick sheaths that are almost completely split so that one set of compact lamellae is surrounded by another set. But despite these alterations in the sheaths, few nerve fibers show axonal degeneration. To quantify the frequency of the age-related alterations in myelin, transversely sectioned nerve fibers from the splenium of the corpus callosum and from the vertical bundles of nerve fibers within area 46 were examined in electron photomicrographs. The material was taken from 19 monkeys, ranging between 5 and 35 years of age. It was found that the frequency of alterations in myelin sheaths from both locations correlates significantly with age. In area 46, the age-related alterations also significantly correlate (P < 0.001) with an overall assessment of impairment in cognition, i.e., the cognitive impairment index, displayed by individual monkeys. The correlation is also significant when only the old monkeys are considered as a group. A similar result was obtained previously in our examination of the effects of age on the myelin sheaths of nerve fibers in primary visual cortex (Peters et al. [2000] J Comp Neurol. 419:364-376). However, in the corpus callosum the myelin alterations correlate significantly with only one component of the cognitive impairment index, namely the delayed nonmatching to sample task with a 2-minute delay. It is proposed that age-related myelin alterations are ubiquitous and that the correlations between their frequency and impairments in cognition occur because the conduction velocity along the affected nerve fibers is reduced, so that the normal timing sequences within neuronal circuits break down.
Peters
Alan
A
Department of Anatomy and Neurobiology, Boston University School of Medicine, 715 Albany Street, Boston, MA 02118, USA. apeters@cajal-1.bu.edu
Sethares
Claire
C
D000375:Aging / Q000473:pathology*; D000818:Animals; D001369:Axons / Q000473:pathology / Q000648:ultrastructure; D001522:Behavior, Animal / Q000502:physiology; D002452:Cell Count; D003072:Cognition Disorders / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D003337:Corpus Callosum / Q000473:pathology* / Q000503:physiopathology / Q000648:ultrastructure; D005260:Female; D007859:Learning Disabilities / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D008253:Macaca mulatta / Q000033:anatomy & histology* / Q000502:physiology; D008297:Male; D008854:Microscopy, Electron; D009410:Nerve Degeneration / Q000209:etiology / Q000473:pathology* / Q000503:physiopathology; D009413:Nerve Fibers, Myelinated / Q000473:pathology* / Q000648:ultrastructure; D017397:Prefrontal Cortex / Q000473:pathology* / Q000503:physiopathology / Q000648:ultrastructure