# Modeling dyslexia in neurotypical adults by combining neuroimaging and neuromodulation techniques: a hypothesis paper

## TL;DR

This paper proposes a new method to model dyslexia in adults using brain imaging and stimulation to better understand and treat the disorder.

## Contribution

The paper introduces a novel two-step approach combining neuroimaging and neuromodulation to model dyslexia subtypes in neurotypical adults.

## Key findings

- Functional and structural MRI can classify dyslexia subtypes based on neuropathological characteristics.
- Transcranial temporal interference stimulation can temporarily induce dyslexic symptoms in neurotypical individuals.
- This model allows for causal investigations into dyslexia subtypes and potential interventions.

## Abstract

Dyslexia is a prevalent developmental disorder marked by deficits in literacy skills. Given that the core deficits of dyslexia are uniquely human, animal models have not been as useful in dyslexia research as they have been in other areas of research. While significant progress has been made through behavioral and neuroimaging studies, a viable model could facilitate controlled investigations into the neural mechanisms underlying dyslexia and accelerate the development of targeted interventions. In this hypothesis article, we propose a two-pronged approach to model dyslexia in neurotypical adults using neuroimaging and neuromodulation techniques. First, we propose using functional and structural MRI data to cluster individuals into neuropathologically derived subgroups in order to facilitate the classification of dyslexia subtypes based on neuropathological characteristics. Second, we propose employing transcranial temporal interference stimulation (tTIS) to temporarily downregulate activity in brain regions specified in the clustering analysis, inducing subtype-specific dyslexic symptoms in neurotypical individuals. This approach enables the establishment of causal or probabilistic relationships between neuropathologies and dyslexia subtypes, while at the same time creating dyslexia models to facilitate investigation into subtype-specific interventions. Although this model is somewhat limited by the transient nature of neuromodulation as well as by the use of healthy adults to model a developmental disorder whose symptoms first arise in childhood, it is a meaningful step towards refining our understanding of the neural basis of dyslexia subtypes and it opens the door to novel and effective therapies. By integrating neuroimaging and neuromodulation, we hope to offer a viable substitute for animal models in dyslexia and accelerate the development of personalized therapeutic strategies for dyslexia.