Today I read a report that once again highlights how our great scientific minds are focusing on epiphenomena rather than the underlying causes. The title is: "Protein Linked To Alzheimer's Disease Also Has Role In HIV Progression." Similarly, one could say, "lack of oxygen linked to being dead." The question is, how helpful are such statements?
Here are the first two sentences from that report: "A protein related to heart disease and Alzheimer's is found to be a factor in HIV. The apolipoprotein (apo) E4 isoform has been implicated in neurodegeneration in Alzheimer's disease, cardiovascular disease, and stroke..."
Source: http://www.sciencedaily.com/releases/2008/06/080616170816.htm
I did an internet search for "apolipoprotein (apo) E4 inflammation" and one of the first few links returned was a study which contained the following statement:
"...apolipoprotein (apo) E4 is much more than a contributing factor to neurodegeneration. ApoE has critical functions in redistributing lipids among CNS cells for normal lipid homeostasis, repairing injured neurons, maintaining synapto-dendritic connections, and scavenging toxins. In multiple pathways affecting neuropathology, including Alzheimer's disease, apoE acts directly or in concert with age, head injury, oxidative stress, ischemia, inflammation, and excess amyloid {beta} peptide production to cause neurological disorders, accelerating progression, altering prognosis, or lowering age of onset..."
Source: http://www.pnas.org/cgi/content/abstract/0600549103v1
Though they make some good points, such as: "...In response to CNS stress or injury, neurons can synthesize apoE. ApoE4 uniquely undergoes neuron-specific proteolysis, resulting in bioactive toxic fragments that enter the cytosol, alter the cytoskeleton, disrupt mitochondrial energy balance, and cause cell death..." a key question involves what one might be able to do to prevent these kinds of "diseases."
Fortunately, one group of scientists do seem to be trying to get at the underlying cause of this particular phenomenon:
"...We showed previously that free radical damage to arachidonic acid (AA) and docosahexaenoic acid (DHA) in brain can be quantified by measuring isoprostanes (IsoPs) and neuroprostanes (NPs), respectively, highly accurate and specific markers of free radical-mediated damage (Roberts et al., 1998; Roberts, 2000). Additionally, because the major isomers of IsoPs and NPs, F-ring or D/E-ring compounds, derive from common endoperoxide intermediates by reduction or isomerization, respectively, the ratio of F- to D/E-ring compounds is a measure of the reducing environment in which oxidation occurred (Reich et al., 2000, 2001). Here we used these quantitative endpoints to test the hypothesis that there is a gene-environment interaction between apoE and alpha -tocopherol with respect to age-related oxidative damage to mouse cerebrum..."
Source: http://www.jneurosci.org/cgi/content/full/21/16/5993
Of course, it would be best is terms like "inflammation" were put aside and instead this kind of molecular-level evidence was viewed with the intention of determining exactly what the sequence of events is. If one does that, the obvious question is, what if we took arachidonic acid and DHA out of our cells, replacing it with the natural, and much less biochemically active, Mead acid? It would not be expensive or difficult (relatively-speaking) to do experiments to determine if ApoE4 is a problem under similar conditions, only with Mead acid in place of AA and/or DHA. My "educated guess" is that the incidence or the age of onset of these kinds of "diseases" would be lowered significantly and raised by many years (probably decades, in many cases, in humans), respectively. I'd even be willing to put up my own money to do such experiments, but only if it turns out that I am wrong here. Who else is willing to "put his money where his mouth is?" |
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