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Researchers at the University of California San Diego have used artificial intelligence to reveal that the PHGDH gene, previously identified as a biomarker for Alzheimer's disease, is actually a direct cause of the condition due to a newly discovered secondary function. According to the study published in Cell and reported by UCSD, this breakthrough not only deepens understanding of spontaneous Alzheimer's but also opens the door to targeted treatments for a disease that affects one in nine people over age 65, writes UCSanDiego Today. (https://today.ucsd.edu/story/ai-helps-unravel-a-cause-of-alzheimers-disease-and-identify-a-therapeutic-candidate)
PHGDH gene's secondary function
Beyond its well-known role in producing the enzyme essential for serine synthesis, PHGDH moonlights as a regulator of gene expression in brain cells-a function previously hidden in plain sight. Using AI to model the protein’s three-dimensional structure, researchers uncovered a DNA-binding substructure that allows PHGDH to activate specific genes, disrupting the delicate balance of gene activity in the brain. This gene regulatory mischief, not its enzymatic duties, triggers a cascade that leads to the early stages of Alzheimer’s disease. The key difference among individuals isn’t whether they have PHGDH, but how much of its protein is produced-higher levels mean more disruption and greater disease progression.
AI modeling of PHGDH structure
Artificial intelligence was the unsung hero in this discovery, acting as both a molecular cartographer and a detective. By predicting the three-dimensional structure of PHGDH with remarkable precision, AI tools revealed a hidden substructure-a DNA-binding domain-that standard protein sequence analysis would have missed entirely. This structural doppelgänger of known transcription factors gave PHGDH its unexpected gene-regulating power, explaining its disruptive influence in Alzheimer’s disease. The AI-driven modeling didn’t just stop at visualization: it enabled researchers to simulate how small molecules might block PHGDH’s rogue regulatory activity, accelerating the search for therapeutic candidates like NCT-503 that target only the problematic function, sparing its essential enzymatic role
NCT-503 as a therapeutic candidate
NCT-503 emerged as a standout small molecule in the hunt for a way to rein in PHGDH’s gene-regulating mischief without sabotaging its vital enzymatic role in serine production. What makes NCT-503 especially attractive is its ability to cross the blood-brain barrier and selectively inhibit PHGDH’s regulatory function, leaving serine synthesis largely unscathed-a crucial distinction for brain health. In mouse models carrying Alzheimer’s-linked mutations, treatment with NCT-503 produced a suite of encouraging results: reduced amyloid plaque buildup, improved memory, and diminished anxiety-like behaviors, all without altering brain serine levels.
The compound’s promise extends beyond symptom relief. By targeting PHGDH “upstream” of amyloid plaque formation, NCT-503 hints at the tantalizing possibility of halting disease progression earlier than current therapies. While the leap from mouse to human remains a formidable one-animal models can’t fully mimic spontaneous Alzheimer’s-these findings position NCT-503 as a leading candidate for further clinical development, and a prime example of how AI-powered drug discovery is accelerating the search for new Alzheimer’s treatments