Why this research

Dementia and the spectrum of neurocognitive decline are on the rise. According to the World Health Organization, in 2017 approximately 50 million individuals worldwide were living with Dementia, and projections suggest that by the year 2030, the number of those affected will reach 82 million. The current pharmacological treatment options have not advanced with the rise of the disease and have not advanced enough to improve quality of life after the onset of symptoms. Early research does point to successful reversal if individualized and comprehensive lifestyle changes and whole system support modalities are initiated in the beginning stages of decline. However, current testing does not support early detection of the disease, thus these changes are difficult to implement and manage after the onset of symptoms and it is often too late.

It is critical that we turn our attention to early detection and diagnostic tools so patients have a chance before symptoms are expressed to reverse or address their underlying factors that lead to chronic inflammation and cognitive decline. Yet, the current Dementia paradigm is misframed; focus is on the secondary pathology that is easily identifiable in the end stage of the disease. This is the  point in the disease process when there is visible and measurable organ damage. We have spent the last 30-40 years trying to prevent this damage rather than understand that it is a compensation for persistent inflammation. As an example, we tend to focus on the tau protein and amyloid deposition, but these are just the body’s attempt to deal with chronic inflammation. These are markers, and they are the archeology of the disease, but are not the cause or original driver of the inflammation. Another example of how the feedback loop of disease can lead us to confuse the body’s compensation patters with causality is in the prevailing hypothesis that mild cognitive decline is vascular, science can easily overlook the deeper understanding the vascular system impairment is also a secondary expression of chronic inflammation. 

Since the cognitive decline processes may be ongoing for decades before signs and symptoms arise, it is imperative to identify the metabolic patterns leading to increased inflammation and expand the window of opportunity for resolving the inflammatory processes that lead to the disease. This would allow for opportunities to interrupt these inflammatory processes before symptoms secondary to chronic neuroinflammation even have a chance to manifest.

About this research

Metabolomics holds great promise in this regard as an early diagnostic tool for Dementia and neurocognitive conditions on the Dementia spectrum. A patient’s Metabolomic profile is like a biochemical roadmap for appropriate patient specific treatment. While genetics might show us predisposition for Dementia, metabolomics are the actual biochemical signaling that show us that the genes are turned on by the environmental milieu. Thus, Metabolomics reveal an individual's unique response to the environment which in turn can inform individualized inflammation-targeted therapies. People with similar patterns of inflammation can be grouped into predictive subtypes and treated prior to what’s possible in today’s current pathological diagnostic model. Additionally, by identifying the metabolomes and inflammatory pathways that lead to the biochemical changes that signal gene expression for Dementia, we have the opportunity to further define the disease spectrum and redefine the nosology for neurocognitive disease.

Where we are now

We are launching an outcomes study to discover the underlying metabolic patterns in patient groups at various stages of cognitive decline. Our core hope is that metabolomics will be able to determine the unique inflammatory patterns that lead to brain inflammation associated with Dementia and diseases on the Dementia spectrum. 

This has the potential to lead to a greater window for addressing cognitive decline and a chance to develop specific treatments to modulate or even resolve the inflammation that caused the decline in the first place. Identifying and interfering with these inflammatory patterns before they become deeply ingrained in compensatory biochemical and physiological processes gives us hope for a future where patients diagnosed with diseases on the Dementia spectrum do not have to face a dead end road.