Surprising sea animals are emerging candidates for modelling human brain diseases 

The process of metamorphosis in Ciona, a type of sea squirt, has molecular similarities to neurodegeneration in humans, according to scientists.  

Ciona is a transparent, sack-like marine invertebrate that survives by filtering in sea waters. This rather odd creature is evolutionarily close to vertebrates and therefore shares a similar nervous system structure during its larvae stage. The neurological similarity, however, begins to break down when Ciona develops into adult form, as it loses elements of its nervous system through neurodegeneration.  

Daniele Capitano, Associate Professor at Laboratory of Proteomics and Separative Sciences in University of Milan, and his team, found in a yet to be published study that the neurodegeneration during metamorphosis of Ciona includes similar molecular changes to brain disorders like Alzheimer’s disease.  

Ciona is useful for studying neurodevelopment because of their simple nervous system structure. Daniele was curious whether the natural loss of neurons in Ciona shared any similarities with human pathological neurodegeneration. 

 “Ciona is an excellent model for these studies because it has a worldwide distribution, has long been used to decipher developmental mechanisms, and offers the scientific community a wide range of experimental tools to investigate these processes in detail” – Daniele said in an email interview. 

Sea squirt picture by Andra Waagmeester.

In the recent paper, proteins extracted from Ciona were separated and then identified using public protein databases that are freely accessible. Their expression levels were compared between different larvae stages, to demonstrate how protein activities change during development. Out of 1152 proteins identified, 405 showed significant changes during the neurodevelopment of Ciona.  

Daniele and his team then consulted past literature that studied protein dysfunctions in human neurodegenerative diseases like Alzheimer’s disease and Parkinson’s disease. By doing so, the team found that proteins affected during neurodevelopment of Ciona were also affected in human neurodegenerative diseases. The study was the first to point out this striking similarity, therefore providing unexpected but convincing evidence that Ciona can be a useful model for human neurodegenerative diseases. 

The study also identified a set of proteins that were not observed in human neurodegenerative diseases, and those that are yet to be characterised. Daniele says that “the most interesting aspect of the research lies precisely here, as within this pool of dysregulated but still unidentified proteins there may be factors that play key roles in human diseases as well.” 

In the future, Daniele and his team will continue to study the proteins with the largest changes in expression during neurodevelopment in Ciona, which may end up being potential targets for early diagnosis and treatment of human neurodegenerative diseases. 

Understanding the mechanism of neurodegenerative diseases is a daunting challenge due to limitations in replicating human conditions using animal models. Expanding the available methods to replicate disease conditions in a laboratory will help scientists tackle one of the most pressing health concerns in the world. 

Written by Kazuma Oura, edited by Marina Milsum.

February 2, 2026.

The preprint can be read here: https://www.biorxiv.org/content/10.64898/2026.01.12.698666v1.full.pdf+html