The Durk Pearson & Sandy Shaw®
Life Extension NewsTM
Volume 18 No. 8 • December 2015

White Matter in the Brain May Be a Key to Degenerative Changes Leading to Alzheimer’s

Recently it has become a focus of much attention in Alzheimer research on the lesions in white matter that are so strongly associated with the disease. White matter is the myelinated tracts that connect neural networks of the brain that are found in gray matter, such as the visuo-spatial processing area that is severely impaired in Alzheimer’s disease. In our last newsletter, Sandy hypothesized that Alzheimer’s might not be a disease where memories are lost, but where the areas containing memories are disconnected from being accessed by other brain areas. If this is the case, then the white matter tracts that constitute these connections might be the key to Alzheimer’s via their vulnerability to damage. White matter lesions have been found in imaging studies of Alzheimer brains and are attracting scientific attention as an important factor, possibly a key factor, in the disease (Godin, 2009; den Heijer, 2006; Stebbins, 2009). Interestingly, depression in older individuals is often accompanied by white matter abnormalities. An earlier paper (Alexopoulos, 2005, cited in Alexopoulos, 2010) proposed that, “white matter abnormalities compromising frontolimbic circuitry may predispose to geriatric depression and interfere with its response to pharmacotherapy.”

One scientist who has done considerable work on the white matter changes in Alzheimer’s disease, George Bartzokis, M.D., has proposed that “white matter may be the primary origin of the complex process that comes to present as AD [Alzheimer’s disease]. That is, white matter involvement may precede, not follow, cortical degeneration. In a series of thoughtful papers, Bartzokis has presented the ‘myelin model’ as an alternative to the traditional conceptualization of the pathogenesis of AD.” “Although still theoretical, the myelin model draws support from many neuroimaging studies.” For example, individuals at familial risk of AD or late onset AD associated with the ApoE4 allele have been found to have white matter abnormalities in memory-related tracts, such as the parahippocampal white matter, cingulum, inferior occipitofrontal fasciculus and splenium of the corpus callosum. “A particularly intriguing DTI study of normal ApOE4 carriers found decreased microstructural integrity of temporal lobe tracts with normal hippocampal and entorhinal cortical volumes.” (quotes in this paragraph come from pp. 305-306 of Christopher M. Filley’s book The Behavioral Neurology of White Matter, 2nd edition, (Oxford University Press, 2012).

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