Tying together spiders' silk, proteins and Alzheimer's dementia
On the evening of Tuesday 6th November, Professor Louise Serpell gave listeners her insight into protein structure and amyloid accumulation – and how this can result in neurodegenerative diseases that continue to cripple our aging population.
Entitled ‘From spider silk to Alzheimer’s disease: Common threads in protein assembly’, Prof. Serpell spoke to a full house in what was her inaugural professorial lecture. It included details of research she and a team of colleagues had carried out in an attempt to study the effect of misfolded amyloid-beta proteins on the nervous system.
A common theory behind the cause of Alzheimer’s is that there is a major fault in the processing of amyloid precursor protein (APP), resulting in a build up of short fragments of APP that can become toxic. The accrual of these short fragments can penetrate neurons, causing them to completely lose their function, which leads to irreplaceable cells dying out. This is what causes many of the well-known symptoms of Alzheimer’s, including memory loss and a confused mental state. By comparing a sufferer’s brain with a normal model, the diminishment of tissue is clear to see, explaining why death is always the end result for an Alzheimer’s patient.
So where do creepy arachnids come into this? Studies have found that a spider’s silk contains amyloid-like nanofibrils, suggesting they must have some way of controlling amyloid assembly, whereas in Alzheimer’s the misfolding and assembly is uncontrolled. It can’t be suggested that spiders control protein production better than humans, as that’s simply not the case. However, what scientists are interested in is how spiders are able to manipulate a specific type of protein aggregation and go on to produce something that’s highly beneficial.
The thought of living in a society where humans are able to control proteins and externally produce useful products with them is as exciting as it is farfetched. More research and understanding of Alzheimer’s disease is critical before any sort of cure can be found, which was emphasised in Prof. Serpell’s lecture. Proteins have a fascinating ability to adapt, having both positive and negative implications on the human body. Although the general structure of proteins has been recognised and studied for many years, the spreading of toxic accumulations in Alzheimer’s is still being researched.
The need for a thorough understanding of Alzheimer’s is perhaps more vital than many think. We live in a world where the average life expectancy is continually rising, and in a country where healthcare is among the best in the world. Consider the fact that in future generations, lifestyle choices and medicine could evolve so dramatically that cancer and heart disease are entirely preventable.
The effects of aging on the nervous system have been proven to be damaging, which is backed up by statistics from Alzheimer’s Society, the UK’s leading research and care charity. They claim that “over a third of people over 95 have dementia”, and predict that it will affect “over a million people by 2021”. For an ever-aging society like our own, these figures are incredibly alarming.
Research is undoubtedly needed, but it’s crucial that this research is carried out in the right areas. Speaking to Prof. Serpell, she agreed that greater knowledge of the disease would be the way to make progress in terms of finding a treatment; and in her lecture posed the suggestion that Alzheimer’s could well be caused by “a one chance event in one cell that can spread throughout the brain”. Learning how this toxicity spans and disturbs the brain will provide clues as to how to go about tackling it.
This issue of funding research in Alzheimer’s has been hotly contested for many years. Alzheimer’s Society alone claim they are forced to “turn down 70 percent of research applications due to [lack of] funding”. This sparks a debate over whether less funding should be given to Alzheimer’s due to its late onset. The need to focus on the root cause of amyloid assembly appears to be the key to unlocking our insight into the cause of disease and it may be the case that studying animals’ control of the assembly could be crucial in enhancing scientists’ understanding of such a complex process