The brain contains white matter, grey matter and black matter. “White matter is composed of bundles of myelinated nerve cell processes (or axons), which connect various grey matter areas (the locations of nerve cell bodies) of the brain to each other, and carry nerve impulses between neurons(ref).” “A 20 year-old male has around 176,000 km of myelinated axons in his brain.” Stretched end-to-end, that would be enough to go around the world more than four times.
Health of white matter in older people seems to be a strong predictor of general functionality and probability of death. A few weeks ago, a report appeared on a “3 year follow-up study of 639 non-disabled older patients (mean age 74.1 (SD 5.0), 45.1% men) in whom brain magnetic resonance imaging showed mild, moderate, or severe age related changes in white matter.” –“The annual rate of transition or death was 10.5%, 15.1%, and 29.5%, respectively, for patients with mild, moderate, or severe age related changes in white matter.” The conclusion of the study was “The three year results of the LADIS study suggest that in older adults who seek medical attention for non-disabling complaints, severe age related changes in white matter independently and strongly predict rapid global functional decline.(ref)”
The relationship between age-related white matter change and serious health problems is multi-faceted. For example, age-related white matter changes stroke death(ref) and such changes negatively affect cognitive functioning(ref).
From an anti-aging viewpoint the three critical questions appear to be 1. What are the typical age-related changes in the white matter? 2. What causes the changes? and 3. What can be done to avert the changes?
As to the first question, one answer is “– the appearance, starting around age 60, of “white-matter lesions” among the brain’s message-carrying axons — significantly affect cognitive function in old age. White-matter lesions are small bright patches that show up on magnetic resonance imaging (MRI) of the brain(ref). The technical term for the change is Leukoaraiosis, involving “changes in the cerebral white matter that can be detected with high frequency by CT and MRI in aged individuals. It is a descriptive term for rarefaction of the white matter. It is also commonly referred to as white matter hyperintensities (WMH) due to its bright white appearance on T2 MRI scans(ref).” Myelin degeneration appears to be another cause of age-related white matter changes(ref). There appears to be a correlation between Leukoaraiosis and small vessel disease.
As to the second question, what exactly causes the white matter changes is only now being established. An earlier hypothysis is that leukoaraiosis may be associated with decreaserd cortical oxygen metabolism(ref). “The result is consistent with the view that primary cortical hypoperfusion (decreased blood flow) plays a role, at least in part, as a pathogenesis of impaired cortical metabolism in hypertensive patients with extensive deep white matter lesions.” That view is also supported by this study. Whatever the basic cause of leukoaraiosis may be, those who have it seem to have decreased regional cerebral blood volume and, most likely, circulation. One research report colorfully states about the cereberal vascular system “Adding to the difficulties, tortuosities develop in some of these vessels with aging. According to some calculations, hypertensive levels of blood pressure would be required to maintain irrigation through some of these vessels.” Also, it appears that “Vascular dementia in leukoaraiosis may be a consequence of capillary loss not only in the lesions, but in normal-appearing white matter and cortex as well.”
Another earlier hypothysis links the white matter lesions with apoptosis(ref). “Nonetheless, because the number of oligodendroglia within the area of leukoaraiosis is greatly depleted, the percentage of cells caught in the act of apoptosis is actually quite high(ref).” A 2009 report links the vascular-defect hypothysis with the apoptosis hypothysis giving a more complete picture. “We explain the vascular changes in LA (leukoaraiosis) as follows. LA induces apoptosis with loss of oligodendrocytes. Capillaries and neuropil are lost. Increased oxygen extraction from the blood in the deep white matter in LA implies that there are too many cells for the remaining capillaries. Thus, the capillaries appear to die first(ref).” Oligodendrocytes play a central role in the white matter. They are a kind of neuroglia cells that provide insulation of and protection for the axons. Oliodendrocytes play a role in the central nervous system similar the role that Schwann cells play in the peripheral nervous system, a topic I discussed in the previous post on Nerve regeneration.
Without going on further about the causes of leukoaraiosis, let me turn to the third question: what can be done to prevent or mimize it? Looking at the causes of this condition it seems that what would help includes:
· Insuring good circulation to the brain. This implies maintaining a healthy vascular system. For practical steps, have a look at my Susceptibility to cardiovascular disease firewall.
· Maintaining healthy oliodendrocytes. This implies continuing regeneration of oliodendrocytes: assuring differentiation of oliodendrocyte progenitor/precursor cells – a partially diffferentiated type of adult stem cell. For a practical approach have a look at the firewall for the Decline in Adult Stem Cell Differentiation theory of aging.
· Maintaining a balanced pattern of oligodendroglial apoptosis. A number of research studies suggest that the effects of TNF-alpha and inflammation often play key roles in initiating unwanted oligodendroglial apoptosis(ref)(ref). “These results demonstrate that aberrant local TNF/p55TNF receptor signaling in the central nervous system can have a potentially major role in the aetiopathogenesis of MS demyelination, particularly in MS subtypes in which oligodendrocyte death is a primary pathological feature, and provide new models for studying the basic mechanisms underlying oligodendrocyte and myelin loss(ref).” Again, practical measures are suggested in the firewall for the Chronic or Excess Inflammation theory of aging. Also inflammatory gene-activation associated with TNF-alpha activation can be inhibited by inhibiting the expression of NF-kappaB, an effect of 36 substances in the combined anti-aging firewall. This topic is discussed as part of the firewall for the Programmed Epigenomic Changes theory of aging.
The bottom line is that the combined anti-aging firewall program should provide protection for the heath of white brain matter in aging individuals. How much protection I cannot say, but it may well be a lot.