Apolipoprotein E (ApoE), a blood test to predict premature cardiovascular and/or Alzheimer’s disease, was prohibitively expensive until June 2010. The Atherotec corp then reduced the price to less than $100 as an add-on study to the VAP (Vertical Atherogenic Profile) which is paid for by most insurance. This would include about 50 other very helpful tests as mundane as a blood sugar to the extremely sophisticated Plac2. This examines for the plaque burden of your arteries as of the moment the blood is drawn.
Regarding the ApoE each of us are given two copies (alleles} of the ApoE at birth and they remain that way lifelong. Therefore the test never has to be repeated again. There is no ApoE e1. We have one each of 2,3, and 4. A person can have e2/e3 or e2/e4 or double of each such as e4/e4. Those with ApoE e2/e2 alleles are at a higher risk of premature vascular disease, although some may never develop disease depending on their lifestyle. Likewise, they may have the disease and not have e2/e2 alleles because it is only one of the factors involved. Our genes cannot change but they can be modified by our diet, exercise and medications. ApoE genotyping adds additional information and, if symptoms are present, e2/e2 can help confirm type III hyperlipoproteinemia a cardiovascular risk factor. This has Chylomicron (Fat/triglyceride globules) remnants and very low density lipoprotein (VLDL) particles which should be rapidly removed from the circulation by the liver. Apolipoprotein E, the main component of the chylomicron and VLDL, binds to a specific receptor on liver cells for disposal. In reference to e2 lipid abnormalities, it will improved lipids with alcohol consumption and there will be little response to diet. With e4, the lipids will improve with a low fat diet. So ApoE is an important determinant of metabolism and treatment of abnormally high lipids.
In addition to predicting age of death ApoE from cardiovascular disease, it predicts
Alzheimer’s(AD), perhaps a fate worse than dying of heart disease. AD is the most common form of dementia. This incurable, degenerative, and terminal disease was first described by German psychiatrist and neuropathologist, Alois Alzheimer in 1906 and was named after him Generally, it is diagnosed in people over 65 years of age, although the less-prevalent early-onset Alzheimer's does occur before this age. In 2010, there were 30.6 million sufferers worldwide. Alzheimer's is predicted to affect 1 in 85 people globally by 2050. And the ApoE test will go a long way to forecast it so you can do things NOW to prolong its onset and even prevent it!
The earliest observable symptoms are often mistakenly thought to be 'age-related' concerns, or manifestations of stress In the early stages, the most commonly recognized symptom is inability to acquire new memories, such as difficulty in recalling recently observed facts. As the disease advances, symptoms include confusion, irritability and aggression, mood swings, language breakdown, long-term memory loss, and the general withdrawal of the sufferer as their senses decline. Gradually, bodily functions are lost, ultimately leading to death. Individual prognosis is difficult to assess, as the duration of the disease varies. AD develops for an indeterminate period of time before becoming fully apparent, and it can progress undiagnosed for years. The mean life expectancy following diagnosis is approximately seven years. Fewer than three percent of individuals live more than fourteen years after diagnosis. When AD is suspected, the diagnosis is usually confirmed with behavioral assessments and cognitive tests, such as a MMSE or a CDR and often I order a MRI looking at the hippocampus volume and if in real doubt a PET scan with a PIB contrast. Individual prognosis is difficult to assess, as the duration and severity of the disease varies much from patient to patient. AD develops for an indeterminate period of time before becoming fully apparent, and it can progress undiagnosed for years. The mean life expectancy following diagnosis is approximately seven years. Fewer than three percent of individuals live more than fourteen years after diagnosis.
Over 60% percent of those who have late onset AD have paired ApoE e4 (e4/e4) alleles. While genetic mutations of the PSEN1, PSEN2, and APP genes are associated with AD in a very small number of specific family lines, they are associated with early onset AD, rather than late onset. The E4 variant is the largest known genetic risk factor for late-onset AD in a variety of ethnic groups. Caucasian and Japanese carriers of 2 E4 alleles have between 10 and 30 times the risk of developing AD by 75 years of age, as compared to those not carrying any E4 alleles. Research suggests an interaction with amyloid. AD is characterized by plaques consisting of amyloid. Apolipoprotein E enhances proteolytic break-down of this peptide, both within and between cells. ApoE-4 is not as efficient as others at catalyzing these reactions resulting in increased vulnerability to Alzheimer's in individuals with this gene. Among ApoE4 carriers, another gene, GAB2, is thought to further influence the risk of getting AD. However, the relationship does not appear as strong as e4, since in the Japanese population, gab2 is not a risk factor. There is also evidence that the ApoE2 allele may serve a protective role in AD. Thus, the genotype most at risk for Alzheimer's disease is ApoE e4/4. The ApoE 3,4 genotype is at increased risk, though not to the degree that those homozygous for ApoE 4 are. The genotype ApoE 3/3 is considered at normal risk for Alzheimer's disease. The genotype ApoE 2/3 is considered at less risk for Alzheimer's disease. Interestingly, people with both a copy of the 2 allele and the 4 allele, ApoE 2/4, are at normal risk similar to the ApoE 3/3 genotype. Other than e4, the other “e s” do get better with Medium Chain Triglyceride Therapysuch as Coconut Oil. Knowing if you are in harms way for either Vascular or Alzheimers disease early in life should give the impetus to change lifestyle. “An enemy known is better than one unknown!”