The effects of normal aging on myelin and nerve fibers: A review

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

ABSTRACT 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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    • "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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    Frontiers in Aging Neuroscience 02/2015; 6. DOI:10.3389/fnagi.2014.00337 · 2.84 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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    NeuroImage 12/2014; 107. DOI:10.1016/j.neuroimage.2014.12.016 · 6.36 Impact Factor
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    • "Importantly, most regions exhibiting decreased fractional anisotropy in combination with increased mean diffusivity in our sample also showed a significant increase in radial diffusivity in the absence of differences in axial diffusivity, which suggests that the major contributor to DTI anomalies in our sample may be myelinrelated pathology (Song et al., 2002). Such an interpretation would also be in-line with the documented effects of normal ageing on myelin integrity, which is known to decrease with advancing age (Peters, 2002). One notable difference with the ageing process, however, has to do with the absence of group differences on the occurrence of age-related white matter hyperintensities in our current sample. "
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