Hi there,
There are many studies about antibody development in AD, however, still effective antibody to AD has not been found. The reasons postulated for this failure are starting time of the treatment and Blood Brain Barrier(BBB).
You know the patients with AD are brought to clinic after AD symptoms observed and unfortunately it is too late to start a effective treatment.
Second hypothesis released to explain the limited success of anti- Aβ antibodies is BBB. it prevents crossing of antibodies to brain.
What do you think about the limited success of antibodies to AD?
Hi Mehmet,
As you have mentioned in the post, the BBB is one of the crucial limiting factor. Aβ is one of the factors that cause AD, and most of the antibody trials were targeting Aβ, but not specifically directed against oligomeric/toxic species of Aβ. Early detection and early therapeutic approach might be helpful.
1 ) It seems that beta amyloide is rather a consequence of AD than the aetiologic main factor. So a clearance of ayloid deposits cdoes not affect evolution of tne disease.
Hi Mehmet,
my point of view about your inquisitive question to get opinions about limited success of antibodies to AD , I propose you to see my last presented work at Croatian Congress on Alzheimer's disease,2014. In Research Gate Lucijan Mohorovic, you can find my Poster Presentation : FERRIC IRON ACCUMULATION IN THE BRAIN - A NEW NANOTECHNOLOGY RESEARCH CHALLENGE.There you can find my long time research interest and, the UCLA study at 2013, which confirm my statement about the role of Ferric iron . SATE OF THE ART explain the recent opinion about the new research needed about the Iron Brain accumulation which is oposit to the standpoint of the current imunological research efforts.I hope that my opinion can at least partly satisfy your dilemma.
.Regards
Lucijan Mohorovic
Robert Moulias, I think that is point should be clarified. The last data in the literature push us to ask the first question again; Aβ is cause or consequence of AD?
This is a question too vast to answer in a simple post. I would advise you to read some of the reviews on the subject. This one in Nature Reviews in Neurology is quite good:
http://www.ncbi.nlm.nih.gov/pubmed/24217510
This one is good too:
http://www.ncbi.nlm.nih.gov/pubmed/24252346
As AD leads to Aβ deposition so only targeting β is not the way to treat AD, For treating it we have to stop the cause behind this. So merely targeting Aβ by β antibody is not sufficient to treat the disease......
I apologize for my complicated discussion above. It is obvious that the immunological approach have limited success of antibody to AD. A-beta brain harmful effects are undeniable conected with ferrous-ferric inversion which has an important part of Alzheimer disease's process.
Many a diseases display a lot of heterogeneity. Same clinical picture can be caused by different factors which cannot be easily identified and hence pathogenesis can be different in different cases of the same disease.Certain infectious agents also induce widely different clinical presentations. Expression of different biological markers also varies in various diseases.Hence, any single therapeutic agent may not work for every case of a disease.
Your coment is significant but is insufficient to answer the question about the limited success of anti-Abeta antibodies to AD.It is well-known the conection with Abeta and ferrous-ferric inversion and the laboratory and clinical effects of this conection but with existent unknowing My point of view is that only red blood cell (RBC) are permanently present in human body from conception to the death and that the methemoglobin (MetHb) is the valuable biomarker and source of the ferric iron an metabolic pathological degradation products .This is the attitude of mind and contribution to the research efforts to explain the sources and causes of the process of pregnancy complication AD, PD.Ms and other neurodegenerative diseases.
There may be several factors at work: (1) there was always a slightly better correlation for tangles, means tau, than beta-A4-amyloid; (2) by definition, the antibodies were given in AD, that means, there is already advanced neurodegeneration corresponding to Braak's stage III or IV. So they may have been given too late in the course of the disease.(3) intrathecal application may be fascinating, but carrying its own risk...
I think that fascination with amyloid in AD , and as a consequence with "anti amyloid" therapy, has something in common with the story of the drunken man who is looking under the lamppost for his keys :" You lost them here ? - No, over there - But why do you look here ? - Because elsewhere I cannot see anything".
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