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MIT researchers uncover more data on gene variant link to Alzheimer’s

Sebastien Bozon/AFP/Getty Images/AFP/Getty Images

In another step toward understanding a terrible disease that threatens many older people’s brains, MIT researchers say they’ve learned more about the possible link between a particular gene variant and Alzheimer’s disease.

MIT neuroscientists performed a “comprehensive study” of the gene variant APOE4, which is three times more common among Alzheimer’s patients than among the general population, the university said in a statement. The researchers also studied the more common form of the gene, APOE3.

The researchers found that APOE4 promotes the accumulation of the beta amyloid proteins that cause the characteristic plaques seen in the brains of Alzheimer’s patients, the university said.


They also found they could eliminate the signs of Alzheimer’s in brain cells in the lab with APOE4 by editing the gene to turn it into the APOE3 variant.

“APOE4 influences every cell type that we studied, to facilitate the development of Alzheimer’s pathology, especially amyloid accumulation,” Li-Huei Tsai, director of MIT’s Picower Institute for Learning and Memory and the senior author of the study, said in the statement.

The research was published Thursday in the online edition of the Journal Neuron. The lead authors were Picower Institute research scientist Yuan-Ta Lin and former post-doctoral student Jinsoo Seo.

If gene-editing technology can be made to work in humans, something many biotech companies are pursuing, the research could lead to a possible therapy, Tsai suggested.

“If you can convert the gene from E4 to E3, a lot of the Alzheimer’s associated characteristics can be diminished,” Tsai says.

The number of people in Massachusetts who have Alzheimer’s and other dementias will increase by 25 percent in just eight years, rising from 120,000 in 2017 to 150,000 in 2025, the Alzheimer’s Association said last fall. Nationwide, 5.7 million Americans are living with Alzheimer’s, the association says.