. Chlamydia pneumoniae induces Alzheimer-like amyloid plaques in brains of BALB/c mice. Neurobiol Aging. 2004 Apr;25(4):419-29. PubMed.

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  1. It is always interesting to see which few of the tens of thousands of weekly science publications catch the eyes of the clever journalists who review these developments for The Economist. The current (March 20-26 2004) issue featured (and cited) the Little et al Neurobiology of Aging paper that revealed evidence of “Alzheimer-like amyloid plaques” in BALB/C mice exposed to Chlamydia pneumoniae via a nasal portal of entry. The authors are more cautious about the interpretation than is perhaps suggested by the article in The Economist, which fails to cite published lines of evidence against the general proposition that this infectious agent may be an etiological agent for late-onset AD. While the authors are a long way from establishing this as a model for Alzheimer’s disease, they should be congratulated for their persistence in pursuing their ideas. I would hope that their future experiments will evaluate the potential impacts of other environmental agents introduced by that route. I am reminded of Dan Perl’s old experiments in which he used a nasal route to show the presence of aluminum in the olfactory system; he got granulomas, not amyloid plaques (Perl et al., 1987).

    References:

    . Uptake of aluminium into central nervous system along nasal-olfactory pathways. Lancet. 1987 May 2;1(8540):1028. PubMed.

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