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Alzheimers Testing

The most common form of dementia, Alzheimer's is a degenerative neurological disorder that leads to memory loss, impaired cognitive function, and eventually death. By 2050 it is predicted that 1 in 85 people will suffer from Alzheimer's disease. There are no available treatments. Early detection allows for symptomatic mitigation.

A key physiological component of Alzheimer's disease is the presence of extracellular plaques, primarily composed of beta amyloid peptides, which aggregate in the brain. These plaques are believed to be toxic and the chief cause of nearby neuron death and cortical material loss. The hippocampus, which plays an important role in short-term memory, is one of the first regions of the brain to suffer damage from Alzheimer's.


A RECENT LANCET NEUROLOGY STUDY OF 44 RELATIVES( aged 18 to 26) , OF ALZHEIMERS PATIENTS showed that 20 had the alzheimers genetic mutation. The deposition of amyloid plaques occured at an average age of 28, about 15 years befor cognitive impairment would be expected and two decades before dementia.

A team of researchers working at the spanish national dna bank has concluded "the apoev4 gene is in fact the main risk factor for developing alzheimers." There are obviously environmenal and other genetic factors which play lesser roles, and the brains ability to control cholesterol levels has a role. Individuals who develop alzheimers go through a transition period and this is the key moment to take mitigating action.


It is now established that alzheimer linked genetic variants begin to damage your brain as early as fifty years before symptoms appear. Early detection allows for optimal mitigation of a future problem.

Alzheimer’s and Genetics

It is estimated that people who have first-degree relatives with Alzheimer’s disease are 4-10 times more likely to develop the disease themselves compared to people with no closely linked family history.

This is particular significant for people with a mother who had Alzheimer’s disease because in that circumstance the disease is even more devastating and results in almost twice as much brain matter being atrophied as all other groups.

Alzheimer’s is a disease with a strong genetic component.

Healthy adults with full cognitive abilities but with certain genetic variants may have differences in their brain, such as the temporal lobe structure. This is indicative of the pre-symtomatic stages of Alzheimer's. Early identification enables appropriate therapy and lifestyle changes in an effort to mitigate the onset of Alzheimer's.

The three major human ApoE isoforms ApoE e2, ApoE e3, ApoEe4 have been linked to differing degrees of onset and severity of Alzheimer’s disease. Our ApoE genome test examines the combination of e2/ e3/ e4/isoforms expressed in an individual’s DNA.

-ApoE e2 is relatively rare and may provide some protection again the disease. If Alzheimer’s disease does occur in a person with this allele it develops later in life than it would in an individual with the ApoE 4 gene.

-ApoE e3 is the most common allele. It is believed to play a neutral role, neither increasing nor decreasing risk.

-ApoE e4 is present in about 40% of all people who develop late-onset Alzheimer’s disease, and in about 30% of the population. People with Alzheimer’s disease are more likely to have an ApoE e4 allele than people who do not develop Alzheimer’s disease, but it can develop even in the absence of the ApoE e4 allele.

ApoE e4 is a risk factor gene because it increases the possibility of developing Alzheimer’s disease. It is important however to remember that some people with one or two ApoE e4 alleles will never get the disease while others who do not have any may develop it.

The Accu-Metric Test Procedure

Collect your DNA sample using the cheek swabs , We will extract the DNA material from the swabs and it will then be amplified in a polymerase chain reaction (PCR). Using a variety of analytical techniques, we will isolate and identify the ApoE gene and its variants, interpret the results , and prepare our report.

A Report of Your Results

Based on the findings of our DNA analysis you will be notified as to which variant of the ApoE gene is present, and the relevant possibilities which you may wish to discuss with your physician.

There are many concerns about whether risk information based upon genetic susceptibility can be properly communicated, and whether such information would benefit or harm those receiving it.

It’s essential to bear in mind that genetic information describes a potential situation that may or may not develop. It is also important to remember that on balance, people have the right to know so they can pursue medical or other advice they deem appropriate.

Genetic variations should be thought of as risk factors and not as certain markers of ultimate disease development.

Alzheimer's and MRI Brain Scans

Over 2000 MRI brain scans have been studied in an effort to establish linkage between brain shrinkage and genetic variants.

The results indicate that persons having the varient ApoE-4-4, which is considered the greatest genetic disposition for Alzheimer's tend to reflect this in changes to affected areas of the brain. The hippocampal region of the brain as well as the amygdala show the greatest deterioration relative to persons who carry variants 2 or 3 of the ApoE gene. The shrinkage and degeneration in an area associated with memory, cognitive and special functions is indicative of a diminishing number of functional braincells and marked synapse loss. ApolipoproteinE (ApoE) participates in the trasport of cholesterol and other lipids, and ApoE4 may interfere with the regeneration of peripheral and central nervous tissue.

Patients whose Alzheimer's test indicate the ApoE-4-4 genotype had smaller volumes of the hippocampus and amygdala than those with other variants.

Your Results

You will be told what your ApoE genetic variants are and their significance in the development of Alzheimer’s disease. Regardless of the results, you should not panic. A genetic predisposition does not necessarily mean that Alzheimer’s disease will result.

You should speak to your health care professional and if symptoms should develop, there are medications that will provide some symptomatic relief.

Resent studies show that the progression of Alzheimer’s disease can be impeded by a number of life style factors. Depending on your results our report will include recommendations in the areas of:

1. Diet
2. Nutritional and other supplements
3. Physical and Mental Activities
4. What to avoid

For example, beta-carotene has demonstrated benefits in impeding cognitive decline. This was confirmed by a study in which 7600 patients were supplemented with 50 mg. of beta-carotene every other day for a year (proceedings of the 9th International Conference on Alzheimer’s disease and Related Disorders).

Our report to you will include various recommendations which you may discus with your healthcare professional.

You can order your no cost, no obligation, sample collection kit by clicking here.

Recent Developments in the Diagnosis of Alzheimer’s Disease

Extensive studies have confirmed that early diagnosis of Alzheimer’s Disease (AD), can be done using fluid obtained from spinal taps. The presence of fragmented beta-amyloid and TAU indicate that the onset of AD has occurred and the individual may already be experiencing mild cognitive impairment.

This new diagnostic tool which may not necessarily be widely used because of a reluctance towards spinal taps nevertheless represents diagnostic progress.

The Viaguard APOE Genetic Scan is designed to determine the degree of vulnerability to AD before any symptomatic evidence, such as beta-amyloid has become evident. The individual may in fact be disease-free but a test result indicating a high degree of vulnerability to AD should initiate dietary and lifestyle changes that may at best impede the onset, but are likely to mitigate the speed of progression.

The APOE Genetic Scan should be considered an invaluable early warning sign.

Recent studies have shown that astrocyte brain cells previously considered as only supportive in a minor role to neurons are in fact very important in enabling neuron function. Lactate released by astrocytes plays a critical role in maintaining long-term memory, as the lactate is an essential fuel to neurons. This finding has major implications for Alzheimer’s disease as methodologies that increase lactate levels have demonstrated positive results in improving long-term memory retention.

It is known that mitochondrial dysfunction plays an important role in the neurodegenerative disorders associated with Alzheimers disease (AD). This dysfunction is triggered by increased levels of Caspase-2 and studies to block this increase and resultant damage are being conducted.

If the Viaguard Alzheimer's apoe gene test indicates a high level of vulnerability to Alzheimer's. You may want to consider discussing with your health care provider the use of zileutyin a drug used for asthma. Researchers at the temple university school of medicine indicate that zileutin blocks 5-lipoxygenase. This enzyme controls the activation of another enzyme - gamma secretase, a prerequisite in the production of amyloid beta.

Amyloid beta deposited in the brain causes neoneural death and resultant dementia/alzheimers.

Beta Amyloid causes neurons in the brain to malfunction and directly contributes to the memory loss that accompanies Alzheimer's progression. We are now beginning to understand the toxic effects of the amyloid protein and its potential for neuro degeneration.

Amyloid protein damages the microtubule transport system responsible for moving chromosomes, proteins, and other cargo inside cells. Microtubules are critical for segregating newly duplicated chromosomes as cell divide. When the duplicated chromosomes cannot separate properly they reassemble inside cells in wrong numbers with an abnormal assortment of genes.

Beta Amyloid proteins are produced by the expression of a gene on chromosome 21 and impede the proper functioning of microtubules in nerve cells causing impaired abilities in connection with learning and memory.

Much research is being dedicated to finding a method to block the production of Beta Amyloid protein which is not only linked to Alzheimer’s but is a causative factor in down syndrome.

Beta amyloid destruction of synapses-the connections that mediate communication between nerve cells-is driven by a chemical modification to an enzyme called Cdk5.

Altered forms of this enzyme are prevelant in AD but not in normal brains.Curent research is looking at ways to inhibit the activity of this enzyme.

Great promise is held out for the oral administration of the cysteine protease inhibitor, E64d, which is safe for humans. This inhibitor not only reduced the build up of beta anyloid plaques in the brain, (the primary cause of alzheimers), but resulted in a substantial improvement in memory.

Understanding the Significance of Genetic Markers

The genetic test that Accu-metrics utilizes for common diseases are risk tests, more analogous to biomarker risk tests such as LDL-cholesterol and PSA, rather than a determinative Mendelian genetic test, such as used for Huntington’s disease.

Another concern is that there may be ethical issues in the introduction of genetic tests for the risk of a disease until all sequence variants that affect the risk of the disease have been discovered. This would be equivalent to claiming that it was wrong to introduce the measurement of cholesterol in assessing its contribution toward the risk of heart attack because it does not account for all the risks. The utility of all risk assessment is dependant on the concern that the results lead to and enable the implementation of preventative or mitigating steps.

In the case of Alzheimer’s, ApoE 4 is the highest risk Alzheimer’s disease susceptibility allele found to date. While studies continue on other contributing genetic factors such as the PCDH11X variants or the PTGS2 gene, the role of ApoE 4 is well established. The importance of detection of a predisposition is that an individual can take steps to address a potential problem, bearing in mind that there is no certainty that they will become a victim of Alzheimer’s.

Accu-metrics believes that DNA based assessment of risk of disease will be a major force in bringing about a paradigm shift from interventional to preventative medicine. Common diseases, such as Alzheimers, occur at the interface of genetics and the environment as both inherited and environmental risk factors play important roles in the disease process. Understanding this genetic component empowers the individual to take extra screening action through lifestyle modification to minimize the likelihood of an inherited predisposition ever developing into disease.

It is implicit in Accu-metrics’ understanding of human rights that no person should be tested for the risk of disease unless they want to be tested.

Is a genetic cure for Alzheimer’s possible?

It has been established that certain genes, to date isolated only in rodents, reduce the formation of amyloid and tau proteins whose deposition as plaques cause tangle formation in brain cells, a precursor to Alzheimer’s disease.

Whereas aggregated beta- amyloid protein forms insoluble clumps between the neurons,the tau protein accumulates inside them.Excess phosphate groups cause the tau protein to malfunction and also form clumps.As a result nutrient transport breaks down, and the neurons and their synapses die off.Tthis stage is accompanied by the early stages of memory loss.

It appears likely that finding a gene or genetic variant in humans that blocks these protein deposits would be a significant advance in the prevention of Alzheimer’s.

These genes work by encoding a protein known as RPS23R1, a stimulant in the production of a further protein GSK-3, which promotes plaque deposition. The search in the human genome for genes that replicate the action of RPS23R1 is being conducted extensively by many research scientists. Should the quest be successful the resultant therapies would be invaluable for those groups of people who have tested positive for certain APOE gene variants detected as a result of the Accu-metrics genetic Alzheimer’s scan.


Current research on the role of Amyloid Plaques indicates although plaques may be present to a limited extent even in normal brains, those plaques tend to be in a more soluble form then those linked to Alzheimers. Other studies have focused on attempts to synthesize anti-bodies that inhibited Amyloid Protein from deposition.


Levels of nitric oxide(NO) a signalling molecule that helps regulate blood flow and neurological processes are low in the brains of people that have or will develop alzheimers.


The amyloid-beta plaques that interfere with brain function have a cell surface receptor that reduces NO signalling ability and initiates neuron degeneration


Alzheimers is the most common form of age related dementia and the most feared disease of old age, because there is no cure. The insidious nature of Alzheimer’s disease is that it begins quietly, unobtrusively, and is not clinically detected as it slowly begins to erode brain networks. This mode of onset is a major reason for the need to identify genetic vulnerability such as certain versions of the APO gene, the basis of this test.


Our Alzheimer scan for identification of genetic vulnerability allows individuals to take the requisite dietary and lifestyle steps that will hopefully slow and mitigate the disease by impeding the development of causative factors such as the formation of plaques and tangles in brain tissue.


There is strong evidence that an insulin degrading enzyme (IDE) produced by genetic expression plays a significant role in breaking down amyloid beta plaque a causative factor in Alzheimer’s. Too little IDE will allow for plaque deposition and the APOE gene variants scanned in the Viaguard Test play a role in this process.


Neurons in the brain are interconnected through long processes called axons. Their functions depend on the transport of diverse material up and down these important pipelines. The most important migratory material is mitochondria, the energy factories of the cell, and the proteins that support cell growth and survival. Amelyoid-beta protein builds up to toxic levels in the brains of people with Alzheimer’s disease and impairs the transport of mitochondria.


Resveratrol increases levels of an enzyme (heme oxygenase) known to protect brain cells from various types of damage, including plaque deposition.


It is not known if it is resveratrol or its metabolites that influence the protective mechanism, but it has been demonstrated that the presence of even minimal levels of resveratrol seems to afford protection from neuronal damage associated with Alzheimer’s.


Natural sources of resveratrol include the skin of red and concord grapes, and any food products that contain them, including red wine.


Studies have shown that Alzheimer's disease is 60-80% heritable, and that the ApoE gene is the dominant gene in this regard. The risk and progress of the disease is measured by neuroimaging, including the volume of the hippocampus, amygdala, and other brain structures. Lifestyle factors including diet impact the degree of onset of the disease.

Are you succumbing to Alzheimer’s?


The normal process of aging is associated with incremental mental degradation that while it may marginally affect cognitive ability is not necessary a precursor to Alzheimer’s disease (AD) unless the process of mild cognitive impairment (MCI) progresses and increasingly affects language and memory. MCI then becomes a precursor to AD with an accompanying decline in the volume of the hippocampal (HC) area of the brain. The HC is responsible for long term memory and special reasoning. While magnetic resonance imaging (MRI) can detect HC atrophy there are other important methodologies.


The free and cued selective reminding test (FCRST) can often discriminate between normal memory change and AD. FCRST consists of the participant being shown a set or 24 images and matching the images with descriptive phrases. Participants are then asked to recall as many images as possible and are given clues for those they fail to remember. There is an analysis done of the number of items remembered and recall times.


While MRI detects qualitative brain changes in the hippocampal region, the impact on any particular individual will be variable. FCSRT allows for a more quantitative verification of the stage of cognitive impairment and is a valuable diagnostic adjunct.


The Linkage Between Alzheimer's and Cardiovascular Disease

Heart attacks and corornary problems are associated with an elevated risk of Alzheimer's and the APOE gene, and others, are known to provide a linkage between Alzheimer's, heart attacks and cardiovascular problems.

This common genetic predisposition has been found in 30% of heart attack sufferers and 40% of those affected by Alzheimer's.

The core of the genetic risk linkage consists of genes that are involved in synthesizing and transporting cholesterol and in controlling the inflammation which is central to both diseases. This means that tests such as the APOE gene detection are not only used to identify the potential for disease, but allow us to define appropriate life-styles to prevent cardiovascular problems and Alzheimer's disease.


Calcineurin 1 regulation is often impaired in down syndrome initiating a process that results in the destruction of neurons in the hippocampus and cortex brain areas.

This is the reason that people with down syndrome (DS) develop Alzheimer's disease (AD) early in life, often in their 30's.

Down Syndrome with a life expectancy of about 49 years, affects about 1 in 800 newborns, and has many similar symptoms to AD in the area of cognitive impairment.

Amyloid plaque deposition is often present in both conditions and the role of the apoe gene and its variants are being studied.


Studies have shown that people who smoke tend to have lower incidences of Alzheimer’s disease and Parkinson's, and have attributed this beneficial effect to nicotine. However nicotine's harmful cardiovascular effects and its addictive proprieties make it a less than ideal choice for treating neurodegenerative diseases.

Research has shown that cotinine, a major by-product of nicotine metabolism and available commercially, does not have the undesirable effects of smoking or nicotine yet tests have shown significant therapeutic benefits.

Extensive studies on animals indicate that cotinine protects neurons, prevents the progress of Alzheimer's disease, enhances memory and is safe. The safety of cotinine has already been demonstrated in its use to relieve tobacco withdrawal symptoms.

Cotinine not only provides a significant reduction in the deposition of amyloid plaques, a causative factor in Alzheimer's disease, but cotinine promotes the survival of neurons and enhances attention and memory.

Cotinine provides another important therapeutic route to impede the progress of Alzheimer's and dementia



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