. Inflammatory responses to amyloidosis in a transgenic mouse model of Alzheimer's disease. Am J Pathol. 2001 Apr;158(4):1345-54. PubMed.


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  1. Timing is everything. This study suggests that COX2 may be upregulated in AD (assuming that animal models are an accurate reflection of the disease) at later stages in the pathogenesis of the disease. Thus, inhibitors of COX2 might be more useful in primary or secondary prevention of the disease.

  2. Association of upregulated C1q with amyloid plaque in Tg mice is worth emphasizing because it has been established to be in AD patient. Thus immunoresponse such as complement must play an important role in amyloid burden.

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