The Greatest Gift You Can Give Your Family Is A Healthy You
Alzheimer’s disease is preventable and potentially reversible in its earliest stages — the medical evidence is very compelling.
Alzheimer’s Disease Prevention: Early Detection of Genetic Predisposition
While Alzheimer’s disease (AD) is commonly associated with cognitive loss, patients often experience symptoms ranging from motor deterioration to behavioral changes. The essential goal of our Alzheimer’s disease prevention program is an early detection of genetic and physiological risk factors that can be managed to significantly modify the progression of late-onset Alzheimer’s disease or prevent its full expression.
Although the primary risk factor for Alzheimer’s disease is advancing age, evidence suggests the gut microbiome influences health well beyond the gastrointestinal tract and may influence the development of neurodegenerative diseases, including Alzheimer’s disease. There is substantial evidence that healthy intestinal microbiota have the ability to positively regulate the neuroimmune responses in the central nervous system. Researchers suspect that bacterial dysbiosis contributes to both gut permeability and blood-brain barrier permeability and ultimately to an adverse neuroinflammatory state — increasing the risk of developing neurodegenerative diseases. (Spielman)
Today, there are specific preventive interventions, based upon individual differences in genes, upon gut microbiome composition, and upon one’s nutritional status, that have been shown to postpone and even reverse early stages of the disease. Moreover, there are evidence-based guidelines for diagnosis and preventive strategies that can be carried out long before an individual has symptoms.
A Prescription for Alzheimer’s Disease Prevention
Our precision medicine program for Alzheimer’s disease integrates breakthrough technological advances, big data science, genomic sequencing, microbiome analysis, blood-based biomarkers, nutrition analysis, neurocognitive testing, and caring support.
Fecal Calprotectin and a Biomarker for Cognitive Decline
A disrupted intestinal barrier is associated with free radical damage to brain tissue and has been found to increase the chances of neurodegeneration — as well as anxiety, depression, and other psychiatric disorders. The intestinal barrier can be disrupted by intestinal inflammation. Fecal calprotectin is an indirect marker of gastrointestinal inflammation. It is most frequently used as a diagnostic tool for distinguishing intestinal bowel disease (IBD) from functional gastrointestinal disorders. It is also observed in other disease states such as celiac disease, colorectal cancer, and gastrointestinal infections. However, emerging evidence suggests that the test can be used to assess cognitive decline. A study carried out on 22 Alzheimer’s patients showed that three-quarters of the patients had elevated fecal calprotectin. Fecal calprotectin may prove to be a valuable biomarker used to diagnose and track the progression of Alzheimer’s disease and other dementias. (Leblhuber)
Other studies have found that administration of Lactobacillus reuteri and Lactobacillus rhamnosus GG, microbiota known to promote gastrointestinal health, was associated with a significant decline in the study subject’s fecal calprotectin compared to the control group.
Two Categories of Genes: Deterministic Genes and Risk Genes
Genes influence whether or not a person develops a disease. People with deterministic genes are certain to develop a specific disease if they live long enough. People with risk genes may or may not develop the disease. However, they are more likely to develop the disease than people without risk genes. Late-onset Alzheimer’s disease falls into this second category.
Early-onset vs. Late-onset Alzheimer’s Disease
Early-onset Alzheimer’s disease is fairly rare — present in less than 5% of all Alzheimer’s disease cases. It afflicts people typically in their 30s, 40s or 50s. The early-onset form is attributed to specific mutations in chromosome 14 and is not preventable.
Late-onset Alzheimer’s is the common form of the disease and has been shown to respond to preventive interventions. It afflicts people typically after age 65. Late-onset risk genes increase the likelihood of developing the disease but do not guarantee that one will get the disease.
Late-onset Alzheimer’s is a Multifactorial Disease
Late-onset Alzheimer’s disease is a multifactorial disease, driven by a multitude of risk genes, environmental exposures, diet and lifestyle factors.
APOE-e4: The Gene Most Correlated with Alzheimer’s
The pathogenesis of Alzheimer’s disease involves multiple genes whose biological effects vary in magnitude. The gene that most commonly correlates with Alzheimer’s is called apolipoprotein E-e4 (APOE-e4). However, assessing single susceptibility genes, such as APOE-e4, to predict one’s genetic risk for developing late-onset Alzheimer’s disease is of very limited value.
Prevention Scientifically Designed Around Your Genome
Across the globe, researchers have worked to identify the spectrum of genes and sequence variations that appear to play the most important role in the development of Alzheimer’s disease. Those research findings now enable the creation of highly personalized programs that match each individual’s genetic risk to a set of evidence-based interventions targeting those risks.
Harnessing Big Datasets To Individualize Your Care
Using large-scale data analysis to decipher genetic risk and harness the vast datasets of biomedical research is what precision medicine is all about. To achieve this, our proprietary artificial intelligence system first identifies your carrier status for the genes whose variations are most strongly associated with Alzheimer’s disease. Next, the system uses a standardized computational method to estimate your genetic susceptibility to developing the disease. Finally, the platform assembles a list of preventive interventions proven to be effective in targeting your at-risk genes.
Addressing the Root Cause of Alzheimer’s Disease
While polygenic risk scoring provides a unique platform to discuss evidence-based preventive recommendations and strives to motivate sustainable lifestyle change, truly personalized medicine requires much more. Addressing the root causes of late-onset Alzheimer’s disease must also include a thorough review of your medical history, physical fitness, microbiome, laboratory biomarkers as well as important evaluation of dietary and lifestyle factors known to interact with those “at-risk” genes.
Spielman LJ, Gibson DL, Klegeris A. Unhealthy gut, unhealthy brain: The role of the intestinal microbiota in neurodegenerative diseases.Neurochem Int. 2018 Aug 13. pii: S0197-0186(18)30198-0. doi: 10.1016/j.neuint.2018.08.005.