Polyphenols in the Protection of Cardiovascular Disease and Dementia

Polyphenols in the Protection of Cardiovascular Disease and Dementia

By Ralph Sanchez, MTCM, CNS

In a recently published study—NutriNet-Santé (10/2018), that included the analysis of dietary records of 84,158 French adults that spanned between May 2009 and June 20017, the higher intake of powerful anti-inflammatory and antioxidant compounds (polyphenols), that are components of a host of foods and beverages found that “Higher intakes of polyphenols, especially of anthocyanins, catechins (flavan-3-ols), and flavonols, were associated with a statistically significant decreased cardiovascular disease risk.”(1). The polyphenol intake was primarily derived from coffee (49%), tea (23%), fruits (17%), vegetables (8%), and wine (5%). (more…)

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

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.
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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 that encodes for TREM 2 protein receptor on microglia, is to aid the brain in efficiently eliminating beta amyloid–the toxic protein that forms plaques associated with Alzheimer’s disease. (more…)

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

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

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.

chronic-inflammation-graphic_large

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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