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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    • "The morphological alterations seen in aging brain are steered by genetic composition of the individuals as well as environmental conditions. Both aging and neurodegenerative disorders share commonalities such as neuronal loss, gliosis, loss of myelination (Peters, 2002), disruption of calcium homeostasis (Nixon, 2003), and so forth. Other features such as neuroinflammation (Sherer et al., 2003), oxidative stress, mitochondrial dysfunction, a-synuclein aggregation, and alteration in protein degradation pathways are reported in PD and aging (Hirsch et al., 2012). "
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    ABSTRACT: Age being a risk factor for Parkinson's disease, assessment of age-related changes in the human substantia nigra may elucidate its pathogenesis. Increase in Marinesco bodies, α-synuclein, free radicals and so forth in the aging nigral neurons are clear indicators of neurodegeneration. Here, we report the glial responses in aging human nigra. The glial numbers were determined on Nissl-stained sections. The expression of glial fibrillary acidic protein, S100β, 2', 3'-cyclic nucleotide 3' phosphodiesterase, and Iba1 was assessed on cryosections of autopsied midbrains by immunohistochemistry and densitometry. The glial counts showed a biphasic increase, of which, the first prominent phase from fetal age to birth could be physiological gliogenesis whereas the second one after middle age may reflect mild age-related gliosis. Astrocytic morphology was altered, but glial fibrillary acidic protein expression increased only mildly. Presence of type-4 microglia suggests possibility of neuroinflammation. Mild reduction in 2', 3'-cyclic nucleotide 3' phosphodiesterase-labeled area denotes subtle demyelination. Stable age-related S100β expression indicates absence of calcium overload. Against the expected prominent gliosis, subtle age-related morphological alterations in human nigral glia attribute them a participatory role in aging.
    Full-text · Article · Aug 2015 · Neurobiology of Aging
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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.
    Full-text · Article · Jul 2015 · Behavioural brain research
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    • "Still today, g-ratio and diameter remain significant tools for the analysis of the myelinated nerve fibers in ''healthy'' peripheral nerves as well as in different types of neuropathies, and in evaluation of the success of the course of post-traumatic regeneration of injured nerve fibers and/or application of different techniques for their reparation. Clinical and experimental studies have shown that the aging is associated with a decline in muscle strength, followed by a decrease in tactile, thermal and vibration sensitivity , as well as significant autonomic dysfunction (Melcangi et al. 2000; Verdu et al. 2000; Peters 2002; Kovačicét al. 2009). So-called senile neuropathy is most frequently accompanied by a decrease in the number and density of myelinated nerve fibers and by numerous irregularities in the myelin sheath. "
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    ABSTRACT: Myelinated nerve fibers suffer from different degrees of atrophy with age. The success of subsequent regeneration varies. The aim of this research was to analyze myelinated fibers of the human sciatic nerve during the aging process. Morphometric analysis was performed on 17 cases with an age range from 9 to 93 years. The outer and inner diameter of 100 randomly selected nerve fibers was measured in each of the cases evaluated, and the g-ratio (axonal diameter/outer diameter of the whole nerve fiber) of each was calculated. Scatter plots of the diameters and g-ratios of the analyzed fibers were then analyzed. Nerve fibers of each case were classified into three groups according to the g-ratio values: group I (g-ratio lower than 0.6), group II (g-ratio from 0.6 to 0.7) and group III (g-ratio higher than 0.7). Afterwards, nerve fibers of group II were further classified into small and large subgroups. The percentages of each group of nerve fibers were computed for each case and these values were used for correlational and bivariate linear regression analysis. The percentage of myelinated nerve fibers with large diameter and optimal g-ratio of the sciatic nerve declines significantly with age. This is accompanied by a simultaneous significant increase in the percentage of small myelinated fibers with g-ratio values close to 1 that occupy the upper left quadrant of the scatter plot. It can be concluded that aging of the sciatic nerve is associated with significant atrophy of large myelinated fibers. Additionally, a significant increase in regenerated nerve fibers with thinner myelin sheath is observed with age, which, together with the large myelinated fiber atrophy, might be the cause of the age-related decline in conduction velocity. A better understanding of the changes in aging peripheral nerves might improve interpretation of their pathological changes, as well as comprehension of their regeneration in individuals of different age.
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