MIT researchers reverse memory loss in mice with Alzheimer's
- 7 years ago
CAMBRIDGE, MASSACHUSETTS — Researchers at MIT have discovered a new potential treatment for Alzheimer's disease which involves the interference of an enzyme that forms blockades in brain cells.
Scientists have discovered that levels of HDAC2 enzyme are usually higher in people with Alzheimer's. Medical mice with the disease also have elevated levels of this enzyme.
HDAC2 binds to a gene called Sp3, which condenses chromatin and reduces the expression of some genes in the DNA that results in blocking memory formation.
Researchers at MIT's Picower Institute for Learning and Memory identified the particular section of HDAC2 that binds to Sp3, and overproduced that fragment. The fragment binds to Sp3, preventing it from binding to entire HDAC2 enzymes, thus allowing the expression of memory-linked genes.
"This is exciting because for the first time we have found a specific mechanism by which HDAC2 regulates synaptic gene expression," Li-Huei Tsai, director of MIT's Picower Institute for Learning and Memory and the study's senior author said in a press release.
Previous attempts at blocking HDAC2 would often trigger dangerous side effects by interfering with the production of red and white blood cells. MIT's technique is the first known procedure to have shown no interference with other enzymes. Researchers are investigating other ways to adapt the technique in human trials.
The study was published in the journal Cell Reports.
Scientists have discovered that levels of HDAC2 enzyme are usually higher in people with Alzheimer's. Medical mice with the disease also have elevated levels of this enzyme.
HDAC2 binds to a gene called Sp3, which condenses chromatin and reduces the expression of some genes in the DNA that results in blocking memory formation.
Researchers at MIT's Picower Institute for Learning and Memory identified the particular section of HDAC2 that binds to Sp3, and overproduced that fragment. The fragment binds to Sp3, preventing it from binding to entire HDAC2 enzymes, thus allowing the expression of memory-linked genes.
"This is exciting because for the first time we have found a specific mechanism by which HDAC2 regulates synaptic gene expression," Li-Huei Tsai, director of MIT's Picower Institute for Learning and Memory and the study's senior author said in a press release.
Previous attempts at blocking HDAC2 would often trigger dangerous side effects by interfering with the production of red and white blood cells. MIT's technique is the first known procedure to have shown no interference with other enzymes. Researchers are investigating other ways to adapt the technique in human trials.
The study was published in the journal Cell Reports.