CyGenica

Computational models

CyGenica uses a non-viral, non-toxic platform to develop in vitro and in vivo delivery solutions for drugs, gene editing components, and antibiotics. CyGenica, focuses on simplifying the patient experience and enhancing their quality of life by enabling safe, targeted, and affordable intracellular delivery of therapeutics. The solution is a non-toxic proprietary engineered negatively charged molecule that works just like a molecular drill. It bores through the cell membrane to deliver molecular cargoes to the nucleus without causing any harm to the cell, thus solving the most crucial issue of targeted intracellular delivery, particularly for targeted Cancer therapy.

It is well-recognized that several cancer therapies can cause alterations to neurocognitive functions. Drug-induced neurotoxicity also has the potential to trigger neurodegeneration and damage to healthy neuronal tissue. With that in mind, it is important to investigate ways to tailor cancer treatments based on their effects in the human nervous system.

Unfortunately, there seems to be a positive correlation between the severity of the pathology and the aggressiveness of the drug used to fight said pathology in the human body which invariably have a significant negative impact on overall quality of life. The importance of personalizing cancer treatment taking into consideration each of the patient’s needs can greatly improve their lifestyle while coping with the disease.

Working with CyGenica, Walton Institute intend to use computational models designed to mimic the neuronal behaviour as accurately as possible when compared to experiments in vitro and in vivo. In addition, information regarding intra- and extra-cellular mechanisms are derived from experiments with neurons in vitro. The idea was to use as much information as we could yield from our simulations to understand how cancer therapeutics can affect the central (CNS) and/or the peripheral nervous systems (PNS).

Evaluation of a normal neuronal communication channel

The goal was to evaluate a normal neuronal communication channel i.e., synapse, and then compare it to potential neurodegeneration that could be directly or indirectly caused by drugs and therapies designed to fight cancer. In other words, the solution is to evaluate the following:

• Research the effects of specific drugs designed to fight cancer aiming to simulate its effects in our computational models.
• Evaluate normal behaviour of a synaptic channel and the propagation of neuronal signals inside a single neuron.
• Apply modifications to neuronal models in order to mimic the drugs side effects and evaluate its impact on neuronal communication.
• Report the performance of each drug from the perspective of neurological functions.

In summary, there is a need for a better and faster way of dealing with the constraints in cancer therapy and, a structured approach in identifying and modelling its neurological manifestations to ensure a safer treatment.

This project aimed to study and quantify the link between cancer therapies and its potential neurological manifestations. We wanted to understand how cancer-therapy-induced neurologic dysfunctions can affect the communication between neurons and, potentially, dictate approaches for a more tailored and less aggressive treatment of carcinogenic entities.

One of the areas of focus of this project was the somatosensory cortex, this is the part of the brain which is not only responsible to receive but also to process sensory information.

This identified further areas of research and the viability to develop novel agents, helping to reduce the potential of damage to healthy neuronal tissues.

The CyGenica & TSSG Technology Gateway partnership

In this way Walton Institute and CyGenica could see out how drugs designed to fight cancer cells can directly or indirectly affect neurons in either the central nervous system (CNS) or the peripheral nervous system (PNS). The ultimate objective was to create a platform where professionals can understand (at least) some of the effects a specific targeted therapeutic can cause in the human nervous system. Our objective at this initial stage of the project was to understand how these drugs can affect the propagation of the neuronal signal through the neuron and the communications between neurons. Using software, we conducted this analysis and the results could then lead to a model that when fed with drug-related data, should be able to estimate any kind of degeneration it may directly or indirectly trigger in the brain.

By tackling the side effects of specific drugs in relation to intra- and extra-cellular mechanisms, we can look for a data-driven approach that could lead to a framework for the analysis and discovery of more tailored and less damaging treatments against cancer, and be a “stepping stone” towards more personalized cancer therapies.