The deposition of Aβ peptides, mainly Aβ40 and Aβ42, in the brain is a key pathological feature of AD and has been proposed as the main pathogenic event in the disease. However, the role played by each of these peptides, and which one is the dominant one in human brain tissue is still a matter of controversy.
Most studies claim that Αβ40 is the dominant peptide species in a normal brain based on plasma and CSF measurements, but this idea is not supported by data from non-diseased human brain tissue, where levels of both soluble and insoluble Αβ40 are lower than those of Αβ42.
On the other hand, most of these studies found that levels of insoluble Αβ40 in Alzheimer’s brains show significantly greater increases over healthy controls than levels of Αβ42.
In addition, it is important to note that β-amyloid depositions in the walls of some cerebral blood vessels that cause cerebral amyloid angiopathy (CAA) are mostly made up of Αβ40 and are associated with an earlier onset of dementia.
Taken together, these data suggest that specific treatment against Αβ40 may be beneficial in certain disease states, which is why we decided to develop a specific active vaccine against this peptide.
vaccine against Aβ40
peptide for the
We believe that specifically targeting the C-terminal end of the Αβ40 peptide can improve the safety profile of the vaccine since the target epitope of ABvac40 can only be recognised and bound by antibodies when the peptide is separated from the cell membrane, preventing the apposition of antigen-antibody complexes on neurons.
In line with this, ABvac40 showed a favourable safety and tolerability profile while yielding a consistent and specific immune response (https://pubmed.ncbi.nlm.nih.gov/29378651)
Additionally, as an active vaccine, the production of ABvac40 is easily scalable and could become a viable treatment to tackle AD, which causes the vast majority of the more than 55 million cases of dementia worldwide (WHO. Dementia. Recover from https://www.who.int/news-room/fact-sheets/detail/dementia)