Peters A. The effects of normal aging on myelin and nerve fibers: a review. J Neurocytol 31: 581-593

Department of Anatomy and Neurobiology, Boston University School of Medicine, 715, Albany Street, Boston, MA 02118, USA.
Journal of Neurocytology (Impact Factor: 1.94). 09/2002; 31(8-9):581-93. DOI: 10.1023/A:1025731309829
Source: PubMed


It was believed that the cause of the cognitive decline exhibited by human and non-human primates during normal aging was a loss of cortical neurons. It is now known that significant numbers of cortical neurons are not lost and other bases for the cognitive decline have been sought. One contributing factor may be changes in nerve fibers. With age some myelin sheaths exhibit degenerative changes, such as the formation of splits containing electron dense cytoplasm, and the formation on myelin balloons. It is suggested that such degenerative changes lead to cognitive decline because they cause changes in conduction velocity, resulting in a disruption of the normal timing in neuronal circuits. Yet as degeneration occurs, other changes, such as the formation of redundant myelin and increasing thickness suggest of sheaths, suggest some myelin formation is continuing during aging. Another indication of this is that oligodendrocytes increase in number with age. In addition to the myelin changes, stereological studies have shown a loss of nerve fibers from the white matter of the cerebral hemispheres of humans, while other studies have shown a loss of nerve fibers from the optic nerves and anterior commissure in monkeys. It is likely that such nerve fiber loss also contributes to cognitive decline, because of the consequent decrease in connections between neurons. Degeneration of myelin itself does not seem to result in microglial cells undertaking phagocytosis. These cells are probably only activated when large numbers of nerve fibers are lost, as can occur in the optic nerve.

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Available from: Alan Peters, Nov 20, 2014
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    • "In normal aging, there arises a weakening of all senses, such as vision [4], audition [5] and somatosensory perception [6] and a decline in motor and executive functions [7]. These declines are accompanied by changes in the peripheral [8] [9] and central nervous systems [10]. Regarding multisensory processing , the parallel presentation of visual stimuli can suppress the activity of other sensory modalities [11] [12]. "
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    ABSTRACT: Visual dominance over other senses is a well-known phenomenon. Closing the eyes, even in complete darkness, can improve somatosensory perception by switching off various aspects of visual dominance. How and if this mechanism is affected by aging remains unknown. We performed detailed neurophysiological and functional MR-imaging on healthy young and elderly participants under the conditions of opened and closed eyes. We found an improved perception threshold in both groups when the eyes were closed, but the improvement was significantly less pronounced in the elderly. fMRI data revealed increased resting activity in the somatosensory cortex with closed eyes, and the stimulus-induced activity of the secondary somatosensory cortex decreased in the young but not in the elderly. This study demonstrates that a switch towards unisensory processing via eye closure is preserved but significantly reduced in the aging brain. We suggest that the decreased ability for unisensory processing is a general phenomenon in the aging brain resulting in a shift toward multisensory integration. Copyright © 2015. Published by Elsevier B.V.
    Behavioural brain research 07/2015; 293. DOI:10.1016/j.bbr.2015.07.014 · 3.03 Impact Factor
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    • "However, age-related alteration of axonal Na + v channel localization in nodal structure and the putative consequences on AP axonal conduction velocity are not known. Age-related changes in myelin structure and composition have been found in the rat corpus callosum (Sugiyama et al., 2002), in mice spiral ganglion neurons (SGNs; Xing et al., 2012), human (Albert, 1993), and non-human primate (Peters, 2002; Sloane et al., 2003). Even though age-related cognitive decline has been suggested to be a consequence of an alteration of the integrity of myelinated axons (Peters et al., 1996; Peters, 2002), whether they also correlate with a reduction in axonal conduction velocity is still unknown. "
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    ABSTRACT: Several studies using vertebrate and invertebrate animal models have shown aging associated changes in brain function. Importantly, changes in soma size, loss or regression of dendrites and dendritic spines and alterations in the expression of neurotransmitter receptors in specific neurons were described. Despite this understanding, how aging impacts intrinsic properties of individual neurons or circuits that govern a defined behavior is yet to be determined. Here we discuss current understanding of specific electrophysiological changes in individual neurons and circuits during aging.
    Frontiers in Aging Neuroscience 02/2015; 6. DOI:10.3389/fnagi.2014.00337 · 4.00 Impact Factor
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    • "Morphology studies consistently reveal declines in striatal/pallidal volume by 4–8% per decade, starting as early as age 20 (e.g., Brabec et al., 2003; Raz et al., 2003; Walhovd et al., 2011; Goodro et al., 2012). Postmortem studies have shown age-related neuronal loss and changes to basic cellular structure such as the myelin sheath in basal ganglia (for reviews, see Haug, 1985; Kemper, 1994; Peters, 2002). Diffusion tensor imaging demonstrated significant age-related reductions in fractional anisotropy and age-related increases in mean diffusivity in the SN and striatum (Cherubini et al., 2009; Vaillancourt et al., 2012). "
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    ABSTRACT: The basal ganglia nuclei are critical for a variety of cognitive and motor functions. Much work has shown age-related structural changes of the basal ganglia. Yet less is known about how the functional interactions of these regions with the cerebral cortex and the cerebellum change throughout the lifespan. Here, we took advantage of a convenient sample and examined resting state functional magnetic resonance imaging data from 250 adults 18 to 49years of age, focusing specifically on the caudate nucleus, pallidum, putamen, and ventral tegmental area/substantia nigra (VTA/SN). There are a few main findings to report. First, with age, caudate head connectivity increased with a large region of ventromedial prefrontal/medial orbitofrontal cortex. Second, across all subjects, pallidum and putamen showed negative connectivity with default mode network (DMN) regions such as the ventromedial prefrontal cortex and posterior cingulate cortex, in support of anticorrelation of the "task-positive" network (TPN) and DMN. This negative connectivity was reduced with age. Furthermore, pallidum, posterior putamen and VTA/SN connectivity to other TPN regions, such as somatomotor cortex, decreased with age. These results highlight a distinct effect of age on cerebral functional connectivity of the dorsal striatum and VTA/SN from young to middle adulthood and may help research investigating the etiologies or monitoring outcomes of neuropsychiatric conditions that implicate dopaminergic dysfunction. Copyright © 2014 Elsevier Inc. All rights reserved.
    NeuroImage 12/2014; 107. DOI:10.1016/j.neuroimage.2014.12.016 · 6.36 Impact Factor
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