Alzheimer’s is one of the most common cause of dementia. Patients with diagnosis usually live on average somewhere between 4-8 years post-diagnosis. As it is a degenerative disease of the mind, patients require increasingly comprehensive care. This care requires vast financial resources with an estimated cost of $355 billion for 2021 in the US alone. The aggregation of tau protein in the patient’s brain is a hallmark of Alzheimer’s disease, and hyperphosphorylation of tau prevents its binding to microtubules in neuronal cells and exposes tau-tau binding sites. Tau monomers aggregate to oligomers (tauO) which then continue to aggregate to paired helical filaments and finally neurofibrillary tangles. Recent discoveries have shown evidence that the actual toxic species is tauO. Therefore, preventing the initial aggregation provides an interesting target for halting or slowing disease progression. We have conjugated a peptide containing an epitope from the proposed binding site to the virus-like particle (VLP) bacteriophage Qβ. Qβ VLPs are protein nanoparticles capable of boosting the immune response to antigens conjugated to their surface. Immunization of mice with our Qβ-based conjugate vaccine produced a stronger immune response than the current gold-standard carrier, keyhole limpet hemocyanin.

Virus-like particle based conjugate vaccine targeting tau aggregation

ACS Spring 2022

The official archive and repository for all ACS Meetings & Expositions abstracts and select posters or presentations.