CSE Enzyme Critical for Memory, Alzheimer’s Link Found
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- CSE deficiency in genetically engineered mice caused memory loss, oxidative stress, DNA damage, and weakened blood‑brain barrier, mirroring Alzheimer’s pathology.
- Bindu Paul led the study that showed CSE‑deficient mice failed the Barnes maze spatial memory test by six months, unlike normal mice.
- Hydrogen sulfide produced by CSE is protective at trace levels, but its toxicity at high concentrations prevents direct therapeutic delivery.
- Solomon Snyder’s earlier work linked CSE to neuroprotection in Huntington’s disease; the new study isolates CSE’s role in Alzheimer’s without other mutations.
- NIH and other funders supported the research, which was published in the Proceedings of the National Academy of Sciences.
Why it matters: If CSE activity can be safely boosted, patients with Alzheimer’s may gain a disease‑modifying therapy that slows cognitive decline, while pharmaceutical companies acquire a new drug target; the study also warns that loss of CSE accelerates neurodegeneration, underscoring the urgency to develop safe ways to maintain trace hydrogen sulfide levels.
