I noticed there are many articles working on this subject, but the method specifically in preparation of Abeta is slightly different from article to article. There were discrepancies about using the solvent, preserving at -20 and the exposure time. I also read somewhere that dependent to where we purchase it the toxicity effect is different.
There have been many attempts to attribute amyloid beta to AD pathogenesis. The premiss is a flawed concept today and now many are turning their attention to tau in the same way they once looked at amyloid and the "pretoxic particles" ADDLs etc. this will result in similar findings as something happens much earlier in this protracted process. I would explore oxidative stress, divalent cations and Fenton and haber-Weiss chemistry. When you do this you will get your answer. Or you could use cytotoxicity assays, comet assay or other apoptosis metrics. Because it's not a necrotic process. Autophagy is a newer concept in AD as well. Good luck
I agree with some of the suggestions from Mark (explore oxidative stress, apoptosis, autophagy), but is also true that the end point of these processes may be also cytotoxicity, so I think is a valid readout. However, I would not say that beta-amyloid hypothesis is a flawed concept. Indeed, seems to me from the literature that tau aggregation is a precess that may be consequence of beta amyloid accumulation.
The exact nature of the toxic form of beta amyloid is still a hot topic, so depending on what you think is right you can prepare purified preparations or just let the peptides oligomerize to get a heterogenic preparation.
Thanks I agree. Finally cell model for sure is not a ultimate answer. Indeed, I did some in vivo experiment and I wanted to go to more details of those affected pathways to show my treatment is indeed neuroprotective . I also noticed some researchers instead of using Abeta itself have used cell lines expressing APP Swedish then examined the Autophagy pathway after their treatment.I am curious to try such model but I haven't found it yet...
Look at the increasingly smaller fragments and peptides Oligomers or ADDLs. I contend its oxidative stress at work before any prodromal stages. Further copper iron and zinc and the various Fenton and Haber Weiss type chemistry are more important in any cytotoxicity assay than the peptides but there is a convention in use. I meant to say that the flawed concept is efforts aimed at removing the plaques by current means which is problematic and I've said that for 15 years and now in retrospect I was right, along with others. Sorry for the confusion if I misspoke. Plaque are probably not good but we should look at earlier changes in this protracted disease process.
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