Current prevalence estimates for late-onset Alzheimer’s disease LOAD in the United States (U.S.) is approximately 5.1 million.(1) By 2050 the projected prevalence of LOAD is expected to escalate to 13.8 million and a staggering 106.8 million worldwide.(2,3) Pharmacological treatments for LOAD such as cholinesterase inhibitors and NMDA receptor antagonists may slow its progression or attenuate specific molecular pathomechanisms associated with the disease process, but are not long term solutions or curative. While there is active research for more effective disease-modifying drugs* the lack of any significant breakthroughs in the treatment of the disease has propelled a paradigm shift away from focusing solely on a pharmaceutical solution to an inclusive prevention model that emphasizes risk reduction and ultimately the portentous global burden incurred by the disease.
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By Ralph Sanchez, L.Ac.,CNS,D.Hom.
The role of chronic inflammation in degenerative disease associated with aging is considered to be a primary vector for the progression of neurodegenative disorders and a powerful factor that underlies their etiology. One needs only to look at the leading causes of mortality, heart disease and stroke, and the research models of inflammation that clearly link it to the pathogenesis and the pathology of these disease processes to understand that inflammation and chronic degenerative disease are inseparable.
Since inflammation is central to aging-associated disease processes, it has been heavily investigated in models of neurodegeneration. In Alzheimer’s disease (AD), the investigation has sought to clarify whether inflammation is a causative stimulus, or a concomitant feature of the disease. Regardless of the etiological focus, the role of chronic inflammation in AD is a well established and the continuing illumination of that knowledge base is vital to the emerging paradigm that seeks to emphasize prevention over a pharmaceutical solution.
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