I'm pretty new to this field. My impression of anti-A beta (e.g. 6E10) antibodies are that they are used more as a stain/marker for either APP, AB40 or AB42 in IHC (Aho et al 2010: http://www.ncbi.nlm.nih.gov/pubmed/20413866).
However, I also read that anti-Ab antibodies are used as a potential therapy in preventing/reducing A beta plaque formation (Thakker et al, 2009: http://www.pnas.org/content/106/11/4501.full).
My dilemma is that if anti-Ab-antibody binding to Ab inactivates it and prevents the formation of A beta plaques, then wouldn't that preclude the use of anti-Ab-antibodies in IHC as stain? i.e. the detection of A beta is also the treatment? In other words, does this mean a good treatment (which would reduce plaques thus less staining appears in IHC) is a bad IHC marker (a bad treatment results in multiple plaques and high A beta concentrations, resulting in abundant staining in IHC?
Read this:
http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0060921
They have some nice results
HI Catalin, thank you for your paper. However, I have read it and it does not answer my question directly. I see that they have used anti-AB bodies to vaccinate the animals but hav einstead used Thiazine red to label the outcomes. Are you suggesting that when anti-AB antibodies are used as a treatment, then they should not be used as a stain for detection?
Scientists find tau protein as better marker of Alzheimer's disease
A buildup of plaque and dysfunctional proteins in the brain are hallmarks of Alzheimer's disease. While much Alzheimer's research has focused on accumulation of the protein amyloid beta, researchers have begun to pay closer attention to another protein, tau, long associated with this disease but not studied as thoroughly, in part, because scientists only recently have developed effective ways to image tau.
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