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News
Scientists have discovered that a primate-specific DNA element can trigger a chain reaction leading to Alzheimer's-like brain damage. Using human brain organoids, Korean researchers found that Alu-mediated gene deletions disrupt zinc balance and Golgi function, causing dramatic increases in amyloid-beta buildup. The findings open a potential new therapeutic target for dementia.
Scientists at South Korea's KRIBB have uncovered a surprising new pathway to dementia — one rooted in a type of DNA sequence unique to primates. Using human brain organoids, the team showed that so-called Alu elements, which make up about 10% of the human genome, can trigger abnormal gene deletions that set off a cascade of cellular damage linked to Alzheimer's disease.
The culprit: when Alu elements cause a deletion in the SPAST gene, it fuses abnormally with a neighboring gene (SLC30A6), slashing levels of ZnT6 — a zinc transporter in the Golgi apparatus. This throws intracellular zinc out of balance, fragments the Golgi, and ultimately drives neurodegeneration. Encouragingly, using a zinc chelator or blocking Golgi fragmentation reversed much of the damage in organoid models.
By the Numbers:
Why it matters: Because mice lack Alu elements, this mechanism has been invisible to traditional animal research. These findings highlight a uniquely human genomic vulnerability and point to the ZnT6–Golgi axis as a promising new drug target for dementia.
