| Description |
Currently, neurological disorders are diagnosed primarily on the basis of patients’ symptoms, and not on the causes of the disease. Furthermore, many symptoms appear in a number of diseases, yet we don’t always know if the causes of a given symptom are the same across diseases or not. Pinpointing the underlying causes of symptoms and diseases is essential if we are to develop targeted treatments for these complex conditions.
IMI’s PRISM project focused on social withdrawal, a common early symptom of many neurological disorders. The “Big Idea” behind the PRISM project is that a quantitative biological approach to the understanding of neuropsychiatric disorders offers major advantages over the principally symptomatic and convention-based approach to diagnostic categorization used at present. PRISM shed new light on the underlying causes of social withdrawal in schizophrenia and Alzheimer’s disease, including some of the genes involved as well as a neural network. Interestingly, the neural network involved in social withdrawal appears to be the same in both diseases. The team also developed an early version of a suite of tests, including scans, blood tests and smartphone monitoring, which could potentially make it easier to diagnose conditions, indicate the brain mechanisms involved, and identify targets for new treatments.
The goal of the PRISM 2 project is to build on the achievements of the original PRISM project. Specifically, it aims to validate PRISM’s findings on social withdrawal in schizophrenia and Alzheimer’s disease, and investigate whether they also apply to major depressive disorder. Ultimately, the work of PRISM 2 should ensure that these findings will result in more accurate diagnoses and treatments for people with Alzheimer’s disease, schizophrenia and major depressive disorder.
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| Objectives |
The overall aim of the PRISM project is to develop a quantitative, transdiagnostic neurobiological approach to the understanding of neuropsychiatric disorders in order to accelerate the discovery and development of better treatments.
Objective 1: To determine the reproducibility of the transdiagnostic and pathophysiological relationship between DMN integrity and social dysfunction in SZ and AD and its potential to generalise to Major Depressive Disorders (MDD).
Objective 2: To test the causality between the quantitative variation in DMN integrity and social dysfunction.
Objective 3: To translate and communicate the project results for the benefit of stakeholders including patients and their families, regulators, health care providers, the general public, learned societies, and the pharmaceutical industry, amongst others. |
