"My research is part of the Mortiboys lab and focuses on the mitochondria – the batteries of our cells - which provide them with enough energy to function and survive. We understand very little about what causes Alzheimer’s disease. One thing we do know is that in cells taken from people with Alzheimer’s, the mitochondria do not function as well as those in cells from healthy people of a similar age, and so are unable to provide enough energy.
My research is trying to understand why this happens, looking specifically at the shape of the network of mitochondria within each cell, how it is altered in Alzheimer’s, and if this is a suitable target for new treatments. Whilst Alzheimer’s is incredibly complex, my work can bring more insight to the specific problem of dysfunctional mitochondria in Alzheimer’s cells, which will better equip us to be able to find potential therapies.
I have always been fascinated by the human brain, the way it works, and the ways in which it can stop working. My interest in Alzheimer’s in particular stems from voluntary work I did in a care home when I was in Sixth Form – seeing the devastating effects Alzheimer’s can have on a person and their family and carers really motivated me to learn more and contribute to finding better treatments.
Previous research published by our lab group has shown that mitochondria in skin cells from people with Alzheimer’s were less functional than in those from healthy people of a similar age. We also showed that the shape of the network of mitochondria is different, with mitochondria being longer and more fused in Alzheimer’s cells.
One of the key processes controlling the shape of the mitochondrial network is the division of mitochondria. We found that a key protein involved in this process, called Drp1, was reduced in cells from people with Alzheimer’s.
My PhD is now building on these findings, by looking more in detail at the division process and the possible reasons for the changes that we see in Drp1. We are initially looking at skin cells from people with Alzheimer’s, my research is also investigating this in brain cells which we have generated from the patient skin cells.
This year we have published a paper showing that some of these changes in the function of the mitochondria are correlated with certain neuropsychological test scores used in the diagnosis of Alzheimer’s, suggesting that changes to the mitochondria contribute to cognitive symptoms."
Katy Barnes
PhD Student, Sheffield Institute for Translational Neuroscience (SITraN)
About World Alzheimer’s Month
World Alzheimer’s Day takes place on the 21st September and is part of World Alzheimer's Month. This year, the campaign aims to highlight the importance of talking about dementia.
Further reading
Bell et al. (2018). Ursodeoxycholic Acid Improves Mitochondrial Function and Redistributes Drp1 in Fibroblasts from Patients with Either Sporadic or Familial Alzheimer's Disease. https://pubmed.ncbi.nlm.nih.gov/30171839/
Bell et al., (2020). Deficits in Mitochondrial Spare Respiratory Capacity Contribute to the Neuropsychological Changes of Alzheimer's Disease. https://pubmed.ncbi.nlm.nih.gov/32365522/