An increasingly accepted hypothesis about Alzheimer’s is that it involves the accumulation of a particular protein known as amyloid beta, which is a peptide of around forty amino acids. In Alzheimer’s patients, two enzymes, beta secretase and gamma secretase, effectively cut amyloid beta segments out of larger, normal parent molecules. These segments damage neurons and synapses and, as they build up, either in soluble form or clumped into plaques, cause the early onset of Alzheimer’s. Some of the processes under development are focused specifically on preventing amyloid beta from being formed in the first place and also try to stop the molecules from attaching to one another if they do form. Once the symptoms of Alzheimer’s, such as memory loss, are evident, a great deal of neurological damage has already been done. Therefore, by monitoring and measuring amyloid beta levels in healthy people before any degradation, the onset of the disease can be detected in advance and remedies applied. Others suggest that “a broader strategy is needed, one that incorporates the role of newly identified genes and even the chemical processes responsible for killing nerve cells.”

By 2020, these and other new developments in genetics and biotechnology are expected to ‘slow the progression of the disease and further alleviate its behavioural and psychological effects’. As a consequence, those diagnosed and treated in the early stages of Alzheimer’s will probably enjoy far greater self-sufficiency than is possible today.

In a similar vein, it is increasingly probable that by 2020 we will also be able to halt the decline of patients with Parkinson’s disease, the degenerative disorder of the central nervous system that impairs the sufferer’s motor skills, speech and other functions. Nearly 1 million people in the US are living with Parkinson’s disease in 2010, again with no known cure but medication or surgery providing relief from the symptoms. By 2030, health forecasts predict up to 9 million patients globally, with around half of these in China. Following recent campaigns, including especially the one led by the actor Michael J. Fox, there has been increased investment and focus on this disease. The big hope here is that stem cell-based techniques will play a big part. One approach being pursued in Sweden involves the removal and cloning of adult neural cells and coaxing them to become dopamine-producing neurons for subsequent re-implantation into patients. Another study underway at Oxford University is using induced pluripotent stem cells taken from a patient’s skin to grow new brain neurons. These and similar studies could well be the next step in cell replacement therapy for Parkinson’s disease.

In the areas of both Alzheimer’s and Parkinson’s, the new developments on the horizon open the door for even longer and more productive lives. In bringing mental degradation under the same control as physical, this could provide an end to the increasingly common situation of the mind degrading faster than the body – and certainly delay the onset of decline.