With decades of experimentation and hundreds of clinical trials, there is still no drug that has been developed that has been shown to improve memory for individuals with Alzheimer’s or other causes of cognitive decline. Researchers have hypothesized that no one answer has been found because chronic common conditions like dementia do not have one etiology, but instead are caused by the effects of a wide variety of genetic variants interacting with each other along with diet, environment and lifestyle.
As the field of genomics has evolved and the fields of functional and integrative medicine have evolved, it is exciting to read about the research showing how dementia can be addressed and even reversed with a precision genomically targeted approach. Examples of how genomics can be used to identify underlying root causes and to develop personalized protocols of nutraceutical, vitamin, lifestyle, and dietary interventions were recently published in Frontiers in Aging Neuroscience.
More About the Publication and Case Studies:
In this proof-of-concept paper, the authors illustrate how genomics was used to identify and target underlying contributing factors of cognitive decline. Patients from various offices across the United States were swabbed for DNA collection and the DNA was then presented back to the patient’s clinician in a format that allowed for improved clinical decision making. The tool utilized in each case, IntellxxDNA™, presented genomics specific to underlying root causes of cognitive decline in a format that made clear the known effects of the particular genomic variant in the literature but also gave genomically targeted potential interventions for each variant. In the clinical decision support (CDS) tool use, in addition to the well-known ApoE 4 variant, hundreds of other genomic variants were presented. These included variants know to interact with ApoE4 and accelerate or decrease the risk conveyed as well as over 100 other genomic variants that can contribute to cognitive decline in their own way. Variants ranged from nutrient carriers, hormone receptors, and variants that conveyed mitochondrial issues or oxidative stress, to variants that affect inflammation, detox pathways, brain ischemia and many more.
One of the issues with the diagnosis of Alzheimer’s that this paper addresses, is that Alzheimer’s disease has become a non-specific diagnosis given to many people with dementia due to a wide variety of etiologies. A study done in 2016 showed that 79% of individuals, who had been given the diagnosis of Alzheimer’s by their neurologists had their diagnosis changed (no longer labeled as Alzheimer’s) when further, more definitive diagnostic testing such as amyloid PET scans were done. n the cases presented in this paper; it becomes clear that there is no one cause of cognitive decline even in Apo E4 individuals. In this paper, all three of the cases studies that are discussed in detail have at least 1 copy of the ApoE4 variant and had been diagnosed with dementia based on cognitive testing. All three got back into the normal range on their cognitive testing within less than a year on a genomically targeted plan – but everyone’s plan was unique and tailored specifically to their needs. Interventions included things like mitochondrial support vitamins, curcumin, citicoline, saffron and methylation support for one individual with a lot of vascular contributing factors to hyperbarics and glutathione, NAC, lion’s mane, and testosterone for another.
Conclusion:
While numerous hypotheses have been tested in the scientific community towards the “cure” for Alzheimer’s and other forms of dementia, to our knowledge, improvements in cognitive measures, especially with the magnitude of improvement seen in these patients who were optimized utilizing genomically targeted interventions, have not been previously reported in studies with any currently available pharmaceutical intervention for cognitive decline. We believe the genomically targeted interventions provide superior outcomes for these patients because cognitive decline is due to many variables, rather than just one.
To get optimal outcomes, the treating clinician needs to be able to first identify which of the plethora of AD risk factors that have been elucidated in the literature are applicable in their patient. Genomics is a powerful tool that can help with this step. The second half of the equation, once identified, is to understand what can be done about each of the potential contributing factors. Taking the contributing factor back to the genomic level helps in identifying modification strategies. A curated genomic Clinical Decision Support platform that identifies the underlying genomics contributing factors can provide a valuable framework for physicians to develop a personalized treatment plan and at a significantly lower cost than traditional treatments that are currently available.
