Research ArticleAlzheimer’s Disease

Amyloid-β peptide protects against microbial infection in mouse and worm models of Alzheimer’s disease

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Science Translational Medicine  25 May 2016:
Vol. 8, Issue 340, pp. 340ra72
DOI: 10.1126/scitranslmed.aaf1059

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  • RE: Remarkable results, questionable report

    “Our findings raise the intriguing possibility that β-amyloid may play a protective role in innate immunity and infectious or sterile inflammatory stimuli may drive amyloidosis” (1). Indeed, fascinating findings. What Kumar et al. did not articulate, though, is that their result is one of many findings, observations, and arguments supporting the theory (2,3) that:

    (i) β-amyloid, tau, α-synuclein, huntingtin, TDP-43, prion protein and other primary proteins implicated in neurodegenerative diseases are members of the innate immune system;

    (ii) The isomeric conformational changes of these proteins and their assembly into various oligomers, plaques, and tangles are not protein misfolding events as defined for decades, nor are they prion-replication activities, but part of their normal, evolutionarily selected innate immune repertoire;

    (iii) The immune reactions and activities associated with the function of these proteins in innate immunity lead to Alzheimer’s, Parkinson’s, Huntington’s, ALS and Creutzfeldt-Jakob Disease, which are innate immunity disorders.

    Generating data and observations, although essential, represents only half of the scientific process; the other is their interpretation and integration into the existing knowledge and paradigms. That’s where the article by Kumar et al. falls short.

    Perhaps the authors were not fully familiar with the literature and paradigms in the field of neurodegenerative diseases. Or, perhaps, Kumar e...

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    Competing Interests: None declared.

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