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Reader Response: Polyphenols in the diet may inhibit development of Alzheimer disease by antibiotic effects on bacteria in the intestinal biome and oral flora

  • Steven R. Brenner, Retired Neurologist, Formerly St. Louis University and the St. Louis VA hospital
Submitted June 04, 2018

I read with interest the Lefèvre-Arbogast et al. article about polyphenyls and reduced incidence of Alzheimer disease (AD). [1] Chronic bacterial infections are associated with development of AD and cause inflammation through activation of innate immunity. [2] The increased permeability of the gut and blood-brain barrier inducted by microbiota dysbiosis may mediate AD pathogenesis and other neurodegenerative disorders, especially if associated with aging. [3] Toll-like receptor 4 is a host defense receptor against invading microorganisms such as bacteria, and is increased in brain tissue associated with amyloid plaque deposition. [4] Plant polyphenols have some antibacterial qualities. [5] Reducing the amount of gram negative bacteria from the GI tract and oral flora from foods containing polyphenols might reduce AD occurrence though inhibiting bacteria and other organisms such as fungi which could contribute to development of AD.

1. Lefevre-Arbogast S, Gadout D, Bensalem J, et al. Pattern of polyphenol intake and the long-term risk of dementia in older persons. Neurology 2018;90:e1979-e1988.
2. Miklossy J, McGeer PL. Common mechanisms involved in Alzheimer’s disease and type 2 diabetes: a key role of chronic bacterial infection and inflammation. Aging (Albany NY) 2016; 8:575-588.
3. Jiang C. Li G. Huang P, Liu Z, Zhao B. The gut microbiota and Alzheimer’s disease. J Alzheimers Dis 2017;58:1-15.
4. Walter S, Letiembre M. Liu Y, et al. Role of the toll-like receptor 4 in neuroinflammation in Alzheimer’s disease. Cell Physiol Biochem 2007;20:947-956.
5. Taguri T, Tanaka T, Kouno I. Antibacterial spectrum of plant polyphenols and extracts depending upon hydroxyphenyl structure. Biol Pharm Bull 2006;29:2226-2235.

For disclosures, please contact the editorial office at journal@neurology.org.

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Neurology | Print ISSN:0028-3878
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