Format

Send to

Choose Destination
Expert Opin Biol Ther. 2019 Jan;19(1):73-78. doi: 10.1080/14712598.2019.1554646. Epub 2018 Dec 17.

A vaccine against Alzheimer`s disease: anything left but faith?

Author information

1
a RIA Immunology, Department of BioMedical Research , University of Bern , Bern , Switzerland.
2
b The Jenner Institute, Nuffield Department of Medicine, The Henry Wellcome Building for Molecular Physiology , University of Oxford , Oxford , UK.
3
c Hypopet AG , Zürich , Switzerland.
4
d Saiba GmbH , Pfäffikon , Switzerland.

Abstract

INTRODUCTION:

Alzheimer's disease looms as a profound and growing threat to future human health. The disease is thought to be primarily driven by aberrant proteolysis of the amyloid precursor protein (APP) and amyloid beta (Aβ) plaque deposition.

AREAS COVERED:

We provide an overview of the molecular pathology that leads to an increase in Aβ peptide accumulation, of the mechanism of action for antibody mediated therapies and of the therapeutic vaccines that target Aβ under development. We also discuss the rationale for using vaccines in the early stages of the disease.

EXPERT OPINION:

The major components of β-amyloid plaques are Aβ1-42 and Aβ1-40 peptides derived from the APP. Reducing these plaques by means of passive or active vaccination against Aβ-peptides has been a long-running endeavor but with disappointing results as the impact on disease progression has been minimal. The data gathered to date could suggest that antibodies do not work, mainly because the studies have not been performed in an optimal fashion. The emerging views are that patients should be treated earlier, ideally in the prodromal or symptom free stage, antibody levels have to be high and the correct epitope must be targeted. More clinical trials to fully explore the potential of vaccines are therefore warranted.

KEYWORDS:

Alzheimer’s; Aβ1-42 Aβ3-6; Virus like particle; vaccine

PMID:
30526133
DOI:
10.1080/14712598.2019.1554646
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Taylor & Francis
Loading ...
Support Center