Prediction of Molecular Links Between Alzheimer's and CSV Disease
Jinah Chung
Wesleyan School,
Publication date: November 20, 2025
Wesleyan School,
Publication date: November 20, 2025
DOI: http://doi.org/10.34614/JIYRC2025II39
ABSTRACT
Alzheimer's disease (AD) and cerebral small vessel disease (CSVD) are devastating neurodegenerative conditions sharing overlapping pathological mechanisms, including vascular dysfunction and inflammation, which contribute to cognitive impairment. The study aims to identify and characterize common protein targets associated with both diseases, which could pave the way for the identification and future development of therapeutics to alleviate symptoms of both conditions. Using five publicly available databases (Ensembl, OMIM, Human Protein Atlas, UniProt, and PubMed), we profiled protein expression patterns in both AD and CSVD. We then analyzed these patterns by developing a protein-protein interaction network using STRING and conducting pathway enrichment analysis. Results highlighted significant enrichment in pathways of locomotion, cell migration, adhesion, axon guidance, and ERK1/2 signaling, suggesting a role in neural connectivity and vascular integrity. Furthermore, an analysis of potential drug targets using EnrichR identified several possible targets associated with existing therapies. Overall, our results provide novel insights into the shared molecular landscape of AD and CSVD, emphasizing the importance of neurovascular interactions in disease progression. The identification of potential drug targets highlights opportunities for drug repurposing to address neurovascular dysfunction in AD and CSVD.
Alzheimer's disease (AD) and cerebral small vessel disease (CSVD) are devastating neurodegenerative conditions sharing overlapping pathological mechanisms, including vascular dysfunction and inflammation, which contribute to cognitive impairment. The study aims to identify and characterize common protein targets associated with both diseases, which could pave the way for the identification and future development of therapeutics to alleviate symptoms of both conditions. Using five publicly available databases (Ensembl, OMIM, Human Protein Atlas, UniProt, and PubMed), we profiled protein expression patterns in both AD and CSVD. We then analyzed these patterns by developing a protein-protein interaction network using STRING and conducting pathway enrichment analysis. Results highlighted significant enrichment in pathways of locomotion, cell migration, adhesion, axon guidance, and ERK1/2 signaling, suggesting a role in neural connectivity and vascular integrity. Furthermore, an analysis of potential drug targets using EnrichR identified several possible targets associated with existing therapies. Overall, our results provide novel insights into the shared molecular landscape of AD and CSVD, emphasizing the importance of neurovascular interactions in disease progression. The identification of potential drug targets highlights opportunities for drug repurposing to address neurovascular dysfunction in AD and CSVD.
