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Cited by 41Alzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration MechanismsDementia and Cognitive Impairment Research

Detection of amyloid beta aggregates in the brain of BALB/c mice after Chlamydia pneumoniae infection

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Boelen, Ellen, Stassen, Frank R. M., van der Ven, André J. A. M., Lemmens, Marijke A. M., Steinbusch, Hellen P. J., Bruggeman, Cathrien A., Schmitz, Christoph, Steinbusch, Harry W. M.·2007·Acta Neuropathologica
DOI 10.1007/s00401-007-0252-3PMC PMC2039821
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Abstract

Neuroinflammation, initiated by cerebral infection, is increasingly postulated as an aetiological factor in neurodegenerative diseases such as Alzheimer's disease (AD). We investigated whether Chlamydia pneumoniae (Cpn) infection results in extracellular aggregation of amyloid beta (Abeta) in BALB/c mice. At 1 week post intranasal infection (p.i.), Cpn DNA was detected predominantly in the olfactory bulbs by PCR, whereas brains at 1 and 3 months p.i. were Cpn negative. At 1 and 3 months p.i., extracellular Abeta immunoreactivity was detected in the brain of Cpn-infected mice but also in the brain of mock-infected mice and mice that were neither Cpn infected nor mock infected. However, these extracellular Abeta aggregates showed morphological differences compared to extracellular Abeta aggregates detected in the brain of transgenic APP751(SL)/PS1(M146L) mice. These data do not unequivocally support the hypothesis that Cpn infection induces the formation of AD-like Abeta plaques in the brain of BALB/c mice, as suggested before. However, future studies are required to resolve these differences and to investigate whether Cpn is indeed an etiological factor in AD pathogenesis.

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  • C. pneumoniae DNA in the olfactory mucosa and olfactory bulb has been detected 1 week after inoculation.

    “After intranasal inoculation in mice, C. pneumoniae antigens and/or infectious organisms have been detected in the olfactory mucosa and the olfactory bulb 1–4 months post intranasal inoculation16–18, and C. pneumoniae DNA in these tissues has been detected 1 week after inoculation18, strongly suggesting that the bacteria can infect the CNS via the olfactory nerve.”

    From Chlamydia pneumoniae can infect the central nervous system via the olfactory and trigeminal nerves and contributes to Alzheimer’s disease risk (2022) · cites this paper as [18]

    The Results section reports C. pneumoniae DNA in the olfactory bulbs of infected mice one week after inoculation. The Methods section lists the brain regions tested but does not include the olfactory mucosa, so this source does not support the claim of detection in both tissues. (LLM, conf=0.88)

    Experimental — accuracy not yet measured

  • C. pneumoniae DNA, antigen and/or live bacteria have been detected in the brain of inoculated mice, which resulted in Aβ deposition or altered appearance of Aβ deposits.

    “C. pneumoniae DNA, antigen and/or live bacteria have been detected in the brain of inoculated mice15–18, which resulted in Aβ deposition16,17 or altered appearance of Aβ deposits18.”

    From Chlamydia pneumoniae can infect the central nervous system via the olfactory and trigeminal nerves and contributes to Alzheimer’s disease risk (2022) · cites this paper as [18]

    The Discussion reports C. pneumoniae DNA in the olfactory bulbs of infected mice one week after inoculation. But it reports nearly identical Aβ immunoreactivity in infected, mock-infected, and uninoculated BALB/c mice, suggesting that the deposits did not directly result from infection. The morphological differences described in the Results are between BALB/c and transgenic mice, not between infected and uninfected BALB/c mice. (LLM, conf=0.88)

    Experimental — accuracy not yet measured

  • After intranasal inoculation in mice, C. pneumoniae antigens and/or infectious organisms have been detected in the olfactory mucosa and the olfactory bulb 1-4 months post intranasal inoculation.

    “After intranasal inoculation in mice, C. pneumoniae antigens and/or infectious organisms have been detected in the olfactory mucosa and the olfactory bulb 1–4 months post intranasal inoculation16–18, and C. pneumoniae DNA in these tissues has been detected 1 week after inoculation18, strongly suggesting that the bacteria can infect the CNS via the olfactory nerve.”

    From Chlamydia pneumoniae can infect the central nervous system via the olfactory and trigeminal nerves and contributes to Alzheimer’s disease risk (2022) · cites this paper as [18]

    The Discussion (page unavailable) reports that Little et al. detected C. pneumoniae in infected mice’s olfactory tissues up to 3 months after inoculation. This paper’s own Results found C. pneumoniae DNA in the olfactory bulb at 1 week, but not at 1 or 3 months; it does not establish detection of antigens or infectious organisms in both named tissues at 1–4 months. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

  • The mice used in these studies were wild-type mice and not mouse models of Alzheimer's disease, suggesting that C. pneumoniae can contribute to the neuropathologies associated with late-onset dementia.

    “Importantly, the mice used in these studies were wild-type mice and not mouse models of Alzheimer’s disease, suggesting that C. pneumoniae can contribute to the neuropathologies associated with late-onset dementia.”

    From Chlamydia pneumoniae can infect the central nervous system via the olfactory and trigeminal nerves and contributes to Alzheimer’s disease risk (2022) · cites this paper as [18]

    The Discussion identifies the infected BALB/c mice as naïve, non-transgenic mice, supporting the wild-type part of the claim. But it reports similar Aβ immunoreactivity in infected and uninfected mice and concludes that the data do not unequivocally support infection-induced AD-like plaques. The proposed contribution to late-onset dementia remains a possibility, not a finding established by this study. (LLM, conf=0.88)

    Experimental — accuracy not yet measured

  • Previous studies have shown that Aβ accumulation after C. pneumoniae inoculation occurs after months.

    “Whilst previous studies have shown that this occurs after months16–18, if the bacteria reach the CNS more rapidly, alterations in Aβ deposition may also occur sooner.”

    From Chlamydia pneumoniae can infect the central nervous system via the olfactory and trigeminal nerves and contributes to Alzheimer’s disease risk (2022) · cites this paper as [18]

    The Results summarized in the paper report extracellular Aβ immunoreactivity at 1 and 3 months after C. pneumoniae inoculation. However, the Discussion says similar immunoreactivity occurred in mock-infected and untreated mice, so this study does not establish that inoculation caused Aβ accumulation. (LLM, conf=0.87)

    Experimental — accuracy not yet measured

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Authors
Boelen, E., Stassen, F. R. M., van der Ven, A. J. A. M., Lemmens, M. A. M., Steinbusch, H. P. J., Bruggeman, C. A., Schmitz, C., & Steinbusch, H. W. M.
Affiliations
Maastricht University (NL)
Corresponding author
Boelen, Ellen
ORCID
Venue
Acta Neuropathologica
Publisher
Springer Science and Business Media LLC
Published
2007-06-21
Volume
114
Issue
3
Pages
255-261
ISSN
  • 0001-6322 (ISSN-L)
  • 1432-0533
DOI
10.1007/s00401-007-0252-3
PMC
PMC2039821
OpenAlex
W2051201119
Cited by
41
References
0
Citations by year
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FWCI
0.63
Type
journal article
Language
en
Open access
Licence
Locations
  • Acta Neuropathologica (publishedVersion, cc-by-nc)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
  • Radboud Repository (Radboud University) (submittedVersion)
Funders
  • Nederlandse Organisatie voor Wetenschappelijk Onderzoek
  • Internationale Stichting Alzheimer Onderzoek
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Keywords
Chlamydia pneumoniae, amyloid-beta, Alzheimer's disease, neuroinflammation, neurodegeneration, bacterial infection, olfactory bulb, APP/PS1 mice, BALB/c mice, amyloid plaques
MeSH terms
Animals, Brain, Female, Humans, Immunohistochemistry, Mice, Inbred BALB C, Mice, Transgenic, Peptide Fragments, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Chlamydophila pneumoniae, Microscopy, Confocal, Neurodegenerative Diseases, Reverse Transcriptase Polymerase Chain Reaction, Chlamydophila Infections, Mice, Plaque, Amyloid

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