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The Alzheimers Solution — Alzheimer’s Disease Prevention and Education

Alzheimer’s Prevention Trials—The Future Looks Promising

Alzheimer’s Prevention Trials—The Future Looks Promising

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.

Several clinical trials have recently explored the potential role of prevention-based interventions for decreasing the risk of late-onset Alzheimer’s disease (LOAD) and vascular dementia. The outcomes are encouraging. Multi-dimensional interventional strategies (implementing multiple treatment and prevention modalities simultaneously) versus mono-therapy (employing only with a single treatment modality e.g. drugs) has yielded promising results in reducing the eventual onset of dementia for aging individuals considered to be at higher risk. These trials highlight the potential effectiveness of preventive approaches for individuals deemed to have a higher risk for vascular dementia and LOAD and for the management of Mild Cognitive Impairment (MCI).**

Oxidative Stress and the Thromboxane Receptor–A Central Pivot in the Production of Neurofibrillary Tangles and Amyloid-beta

Oxidative Stress and the Thromboxane Receptor–A Central Pivot in the Production of Neurofibrillary Tangles and Amyloid-beta

By Ralph Sanchez, MTCM, CNS, D.Hom.

New research published Oct. 13 by the journal Neurobiology of Aging revealed that the free radicals produced during oxidative stress bind to a protein receptor in the brain designated as “the Thromboxane Receptor A2 (TP)”. The study, “Modulation of AD Neuropathology and Memory Impairments by the Isoprostane F2α Is Mediated by the Thromboxane Receptor” demonstrated that oxygen free radicals actually bind to TP, and transmit signals to neuronal cells to increase the production of amyloid beta, and Neurofibrillary Tangles (abnormal phosphorylated microtubule-associated protein tau), the two major pathological lesions associated with Alzheimer’s disease. See illustration just below.

TREM2 gene mutation raises the risk of Alzheimer’s disease

TREM2 gene mutation raises the risk of Alzheimer’s disease

By Ralph Sanchez, MTCM, CNS, D.Hom.

Recently (11/13), a rare variant of the TREM2 gene, designated as R47H, was shown to increase the risk of developing Alzheimer’s disease. Individuals with the variant may be up to 3 to 5 times more likely to develop Late Onset Alzheimer’s disease (LOAD). This susceptibility to LOAD in R47H genotypes, is similar to that conferred by the ApoE4 gene.

The TREM2 gene is involved in immune regulatory processes in the brain and the R47H mutation impairs the gene’s ability to contain inflammation. One of the roles of the TREM2 gene is to aid the brain in efficiently eliminating beta amyloid; the toxic protein that forms plaques associated with Alzheimer’s disease.

Inflammation and Alzheimer’s Disease—Cause, or Effect?

Inflammation and Alzheimer’s Disease—Cause, or Effect?

The role of chronic inflammation in degenerative disease associated with aging, is considered to be a primary vector for the progression of said diseases, 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 degenerative 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, inflammation in AD is a well established entity, and the continuing illumination of that knowledge base, is vital to our intent to hopefully prevent, delay, or to develop medical strategies for treatment.



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Reader Testimonials

“What a tremendous resource! Thank you for putting all of this great research in one place! I am also extremely interested in warding off a family history of Alzheimer’s and Dementia. Medicine can be so very powerful when we are able to identify the biochemical inefficiencies, apply specific dietary and nutritional remedies and compile a protocol to heal not just an individual, but generations. Thank you Ralph!”

“Absolutely the BEST article I have read on the insulin/AD connection. As always, your brilliance is very much appreciated!”

“This is an incredible article! Very powerful information! Thank you so much for putting it together the way that you have. This information needs to get out to the masses. You explained that very well.”

“Thank you so much for this well written article. Looking forward to future updates. Thanks for this well illustrated, researched, and detailed yet succinct article.”

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