‘When we see this effect on prion infections, we believe the same approach could work on Alzheimer’s disease as well,’ says Peter Nilsson, a researcher in Bioorganic Chemistry funded by the European Research Council (ERC).
Prion disease is a group of progressive conditions that affect the brain and nervous system of humans and animals. Human prion diseases include sporadic Creutzfeldt-Jakob disease, Kuru, variant Creutzfeldt-Jakob disease, Gerstmann-Sträussler-Scheinker syndrome, and fatal familial insomnia. Prion illnesses can be inherited, occur spontaneously or through infection, for example through infected meat – as was the case with mad cow disease.
‘Based on these results, we can now customise entirely new molecules with potentially even better effect,’ Dr Nilsson said.
Researchers want to go even further and test whether the molecules will function on fruit flies with an Alzheimer’s-like nerve disorder. Alzheimer’s is caused by what is known as amyloid plaque, which has a similar but slower course than prion diseases.
The EU-funded LUPAS project, meanwhile, sought to bridge the gap between diagnosis and treatment of Alzheimer disease and prion diseases. At the beginning of the project the LUPAS team believed that by developing novel agents and methods for diagnostic imaging of amyloid plaque it would be possible to improve quality of diagnosis and facilitate monitoring and understanding of the disease progression.
The project gathered partners from a wide range of areas ranging from experts within organic synthetic chemistry, synthetic nano chemistry, amyloid structure, prion disease, Alzheimer’s disease, magnetic resonance imaging, multi-photon physics and hyper spectral imaging. They formed the critical mass of competences needed to reach towards the project’s ambitious goals.
LUPAS coordinator Professor Per Hammarstrom said at the launch of the project: ‘The competence within the LUPAS consortium will undoubtedly bring forward novel tools for understanding the pathological hallmarks of Alzheimer’s disease and prionoses. Within the three-year timeframe of LUPAS we will develop these tools for use in disease models systems in vivo and on histolological ex vivo samples from humans. If successful it will take a few more years to apply this technology in the clinic.’