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Novel dementia vaccine on track for human trials within two years:
A newly published study has described the successful results in mice of a novel vaccine designed to prevent neurodegeneration associated with Alzheimer's disease. The researchers suggest this "dementia vaccine" is now ready for human trials, and if successful could become the "breakthrough of the next decade."
The new study, led by the Institute for Molecular Medicine and University of California, Irvine, describes the effect of a vaccine designed to generate antibodies that both prevent, and remove, the aggregation of amyloid and tau proteins in the brain. The accumulation of these two proteins is thought to be the primary pathological cause of neurodegeneration associated with Alzheimer's disease.
The research revealed the vaccine led to significant decreases in both tau and amyloid accumulation in the brains of bigenic mice engineered to exhibit aggregations of these toxic proteins. Many prior failed Alzheimer's treatments over the past few years have focused individually on either amyloid or tau protein reductions, but growing evidence suggests a synergistic relationship between the two toxic proteins may be driving neurodegeneration. Hence the hypothesis a combination therapy may be the most effective way to prevent this kind of dementia.
This new treatment combines two vaccines, dubbed AV-1959R and AV-1980R, which are designed to respectively target amyloid and tau protein aggregations. The vaccine is formulated in a novel adjuvant called Advax, developed by a team of Australian researchers to enhance vaccine immunogenicity.
Advax has been developed by Nikolai Petrovsky, a scientist from Australia's Flinders University who told ABC News Australia the new formulation offers the potential to act as both a preventative vaccine against the development of neurodegeneration, and a curative treatment in subjects already suffering from a build-up of these toxic proteins.
[...] The new research was published in the journal Alzheimer's Research & Therapy.
(Score: 1, Informative) by Anonymous Coward on Monday January 06 2020, @05:52PM
>Any links to these findings?
https://www.medpagetoday.com/meetingcoverage/aaic/52705 [medpagetoday.com]
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3693547/ [nih.gov]
And meanwhile https://alzres.biomedcentral.com/articles/10.1186/alzrt269 [biomedcentral.com] :
"Most disease-modifying trials have some form of Aβ protein as the pharmacologic target (that is, four of six current Phase 3 compounds of disease-modifying agents target the amyloid-beta protein). One-hundred forty-five (65.6%) of 221 trials of disease-modifying agents registered in the 2002 through 2012 period were directed at this target. The target is unvalidated, and no class of agents has shown efficacy for this target in human clinical trials. Many animal models of amyloidosis have shown biological and behavioral benefit from anti-Aβ agents, creating a “translational gap” between human and animal studies [27–30]."
"The definition of insanity is doing the same thing over and over again and expecting a different result."
P.S.: If https://doi.org/10.1016/j.neuron.2018.06.030 [doi.org] is correct in that, the Aβ protein serves a *defensive* role against the underlying infection. End results of a treatment designed to remove it, are easy to deduce if that is the case.