If the brain can be supplied with information, sight can be restored and to make the necessary connections, diamonds offer one of the best solutions.
Prof Masserini’s team, now half way through the five-year project, have already succeeded in designing multi-functionalised liposomes that meet these three criteria. Tested on cell cultures – that is on cells that are grown in vitro (e.g. co-cultures of endothelial cells and glial cells), these liposomes have already demonstrated their ability to pass the blood-brain barrier, bind to and neutralise the beta-amyloid proteins. Now the team is testing their nanoparticles on transgenic mice with a disease resembling Alzheimer’s (called animal models of Alzheimer’s). The results so far are positive. Once injected in the mice, the liposomes could remove the amyloid beta from the blood and decrease their content in the brain. Will that be enough to improve the mice’s condition? This is the key question. There has been an on-going controversy about what is actually causing Alzheimer’s. Prof Masserini himself is quite convinced of the role of the beta amyloid proteins in the development of the disease. While beta amyloid might not be toxic at the beginning (and may be even beneficial according to some evidence), progressively, as Alzheimer’s develops, their accumulation becomes toxic and is responsible for the death of nearby neurons. But as Alzheimer’s takes time to develop, assessing any potential cure also takes time. Prof Masserini and his collaborators still have 2.5 years ahead of them to check whether the treatment is able to reverse Alzheimer’s in transgenic mice, and eventually in humans. ”Alzheimer’s affects more than 24 million people in the world with one new case every seven seconds,” said Prof Masserini. In Europe the number of people with Alzheimer’s is expected to double to reach more than six million by 2040. So there is a significant challenge to find a cure before then.
NanoEar Regenerating the ear and the eye
NANOTEchNOlOgy could also revolutionise the management of some of the most disabling diseases, including hearing deficit and blindness. According to Ilmaru Pyykkö, from the University of Tampere, Finland, hearing deficit is the ninth most severe disease in the EU, surpassing even blindness (the 16th) with more than 250,000 deaf people and 13 percent of the European population with bad hearing. “The medical prevention and treatment is restricted by the fact that the inner ear is difficult to access as it is buried deep in the temporal bone and isolated from circulation by tight barriers,” Prof Pyykko explained. here again, production of targeted multifunctional nanoparticles may provide a solution and improve the life of thousands of sufferers. The idea is that nanoparticules inserted in cochlear implants will carry and release drug/gene precisely to targeted tissue sites and selected cells in the inner ear. Prof Pyykko described the potential benefits: “The problem with cochlear implants is that people get completely lost when there is a background noise; they can’t even listen to music as it is painful for their ears,” he said. Nanoparticles introduced with the implant could stimulate nerve growth factors and therefore encourage the connection between nerve cells and
electrodes, resulting in improved hearing. There are no less than 23 people working on what has been called the ‘NANOEAR consortium’. Still, according to Prof Pyykko, this technique might take a couple of years to achieve reliable results and get translated to the clinical practice.
DREAMS
The development of blindness with age is very common. Age-related visual loss is typically caused by a condition called age-related macular degeneration (AMD), whereby the retina becomes detached, resulting in a loss of vision in the centre of the visual field (macula) – making it difficult or impossible for sufferers to read or recognise faces. There is another retina disease, called retina pigmentosa (RP), which is characterised by the degeneration of photoreceptors at the back of the retina, and also results in vision loss but this time around the periphery rather than at the centre. AMD and RP have something in common which comes handy in the fight against these diseases: they only affect retina cells and not the neuronal cells that are in charge of the transmission of the signal from the retina to the visual cortex. This means that by stimulating the nerve cells directly in the same way the retina does, it should be possible to make an AMD or RP patient see again. Researchers are thus looking for the ideal retinal interface for sending electric signals to the optic nerve: one that’s both photosensitive and biocompatible.
SCIENCE SPIN Issue 48 Page 28