Detection of amyloid beta aggregates in the brain of BALB/c mice after Chlamydia pneumoniae infection.
Detection of amyloid beta aggregates in the brain of BALB/c mice after Chlamydia pneumoniae infection.
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肺炎衣原体感染后,检测BALB/C小鼠大脑中淀粉样蛋白β骨料。
DOI:
10.1007/s00401-007-0252-3
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发表时间:
2007-09
影响因子:
12.7
通讯作者:
Steinbusch, Harry W. M.
中科院分区:
文献类型:
--
作者:
Boelen, Ellen;Stassen, Frank R. M.;van der Ven, Andr J. A. M.;Lemmens, Marijke A. M.;Steinbusch, Hellen P. J.;Bruggeman, Cathrien A.;Schmitz, Christoph;Steinbusch, Harry W. M.
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 (Aβ) 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 Aβ 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 Aβ aggregates showed morphological differences compared to extracellular Aβ aggregates detected in the brain of transgenic APP751SL/PS1M146L mice. These data do not unequivocally support the hypothesis that Cpn infection induces the formation of AD-like Aβ 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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影响因子:
4.2
作者:
Boelen, Ellen;Steinbusch, Harry W. M.;Stassen, Frank R. M.
通讯作者:
Stassen, Frank R. M.
影响因子:
9.9
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Kuo, CC
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5.4
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Hudson, AP
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通讯作者:
Maass, M
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6.4
作者:
GRAYSTON, JT;ALDOUS, MB;ALTMAN, J
通讯作者:
ALTMAN, J