Date Published:
2025 Feb

Publication Type:
Journal Article

Authors:

Eric J Barnett
Jonathan L Hess
Jiahui Hou
Valentina Escott-Price
Christine Fennema-Notestine
William Kremen
Shu-Ju Lin
Chunling Zhang
Chris Gaiteri
Jeremy Elman
Peter Holmans
Stephen V Faraone
Stephen J Glatt

PMID:
40061341

URL:
https://pubmed.ncbi.nlm.nih.gov/40061341/

DOI:
10.1101/2025.02.26.25322962

Abstract:
Background: Genetic risk factors for psychiatric and neurodegenerative disorders are well documented. However, some individuals with high genetic risk remain unaffected, and the mechanisms underlying such resilience remain poorly understood. The presence of protective resilience factors that mitigate risk could help explain the disconnect between predicted risk and reality, particularly for brain disorders, where genetic contributions are substantial but incompletely understood. Identifying and studying resilience factors could improve our understanding of pathology, enhance risk prediction, and inform preventive measures or treatment strategies. However, such efforts are complicated by the difficulty of identifying resilience that is separable from low risk. Methods: We developed a novel adversarial multi-task neural network model to detect genetic resilience markers. The model learns to separate high-risk unaffected individuals from affected individuals at similar risk while "unlearning" patterns found in low-risk groups using adversarial learning. In simulated and existing Alzheimer's disease (AD) datasets, we identified markers of resilience with a feature-importance-based approach that prioritized specificity, generated resilience scores, and analyzed associations with polygenic risk scores (PRS). Results: In simulations, our model had high specificity and moderate sensitivity in identifying resilience markers, outperforming traditional approaches. Applied to AD data, the model generated genetic resilience scores protective against AD and independent of PRS. We identified five resilience-associated SNPs, including known AD-associated variants, underscoring their potential involvement in risk/resilience interactions. Conclusions: Our methods of modeling and evaluation of feature-importance successfully identified resilience markers that were obscured in previous work. The high specificity of our model provides high confidence that these markers reflect resilience and not simply low risk. Our findings support the utility of resilience scores in modifying risk predictions, particularly for high-risk groups. Expanding this method could aid in understanding resilience mechanisms, potentially improving diagnosis, prevention, and treatment strategies for AD and other complex brain disorders.