ApoE4 and its fragments impair mitochondrial functionThus, apoE4 may cause mitochondrial dysfunction at very early stages in life.
http://labs.gladstone.ucsf.edu/huang/pa ... e-research
Mitochondrial Disease is, of course, a separate entity from what E4 carriers experience; but I decided to take a look and see if I saw any overlap.Mitochondrial dysfunction has been reported in AD, which is modulated by apoE genotype, with a greater effect in apoE4 than in apoE3 carriers [121-124,125]. In both AD patients and age-matched nondemented subjects, apoE4 is associated with decreased cerebral glucose metabolism [126-135], an effect that occurs decades before cognitive impairment become apparent [126,127,136] and, probably, also before significant Aβ deposition. Thus, apoE4 may cause mitochondrial dysfunction at very early stages in life. Mitochondrial dysfunction is clearly coupled with production of reactive oxygen species and increased oxidative damage, which in turn further impair mitochondrial activity. Temporary or sustained loss of mitochondrial function impairs cellular defenses and repair mechanisms, decreasing the ability of neurons to mount an appropriate stress response and causing cellular injury.
What is mitochodrial disease?
http://www.umdf.org/site/c.8qKOJ0MvF7LU ... isease.htm
Symptoms of mitochondrial disease:
http://www.umdf.org/site/pp.aspx?c=8qKO ... &b=7934631
Perhaps I'm unique, but this 4/4 has experienced 17 of the 38 symptoms This feels significant to me. Mitochondrial dysfunction in Alzheimer's is well studied, but there is increasing evidence that mitochondrial damage/dysfunction occurs both in normal aging and in atherosclerosis. And, no surprise, E4 carriers are more dramatically affected.
Here's an interesting study in which APOE null mice (commonly used in atherosclerotic research, somewhat synonymous with E4 humans) demonstrated early widespread mitochondrial damage in vessel walls. The mitochondrial deficiency was found was to promote atherogenesis and was not a consequence of tissue damage.
Mitochondrial DNA Damage can Promote Atherosclerosis Independently of Reactive Oxygen Species and Correlates with Higher Risk Plaques in Humans
Addressing mitochondrial dysfunction MAY be one of our most important strategies for preventing both AD and CAD.