Does brain trauma cause premature ageing of the nervous system?

Award Number
Status / Stage
1 July 2022 -
30 June 2025
Duration (calculated)
02 years 11 months
Funding Amount
Funder/Grant study page
Contracted Centre
University of Liverpool
Principal Investigator
Dr Natalia Sanchez-Soriano
PI Contact
WHO Catergories
Models of Disease
Understanding Underlying Disease
Disease Type
Cognitive Impairment

CPEC Review Info
Reference ID377
ResearcherReside Team


Award NumberBB/W016907/1
Status / StageActive
Start Date20220701
End Date20250630
Duration (calculated) 02 years 11 months
Funder/Grant study pageBBSRC UKRI
Contracted CentreUniversity of Liverpool
Funding Amount£524,794.00


Mild head trauma can lead to long-term post-traumatic processes that resemble cognitive decline during ageing. This suggests that trauma may accelerate ageing and share common patho-mechanisms. However, there is an incomplete understanding of the cell biological mechanisms that cause post-traumatic brain deterioration. Here we will research the cell biological processes induced by mild trauma and compare them to the ageing brain. We will use our newly established in vivo model of mild repetitive trauma in Drosophila, which allows subcellular studies of identified cells and can be combined with our ongoing ageing studies. Capitalising on the powerful genetic approaches and quantifiable readouts provided by this model, we observe that trauma prematurely induces phenotypes well known to us from our work on the ageing brain. This includes the atrophy of axons and synapses, alterations of the microtubule cytoskeleton and changes in the distribution and morphology of organelles. We hypothesise that mild trauma causes later-onset organelle and axonal damage, initially triggered by axonal microtubule deregulation causing transport defects and, in turn, detrimental organelle dysfunction. This cascade of patho-mechanisms appears to be shared by trauma and ageing. We will study the mechanisms linking trauma to microtubule aberration, the knock-on effects on organelles and neuronal physiology, and stablish cytoskeletal manipulations as neuroprotective strategies. We will establish commonalities between the cell biology of trauma and ageing. We will use interventions known to delay ageing and test whether these improve trauma pathology. Throughout, we will use a combination of genetics, biochemistry, immunohistochemistry, proteomics and in vivo imaging. We expect the outcomes derived from our work to provide important understanding applicable in translational research, with implications also for research into ageing.