Web Desk(October 11, 2017): Researchers found that removal of the regulatory gene LSD1 in adult mice induces changes in gene activity similar to Alzheimer’s disease.
The study, published today in Nature Communications, showed that lysine specific histone demethylase, or LSD1, is agitated in brain samples of people with Alzheimer’s disease and frontotemporal dementia.
The findings in human patients and mice show that LSD1 plays a central role in neurodegenerative diseases like Alzheimer’s and could lead to a possible drug target.
When researchers engineered mice that have LSD1 taken out in adulthood, the mice became paralyzed and cognitively impaired.
The mice, however, lacked aggregated proteins in their brains thought to play a significant role in Alzheimer’s and FTD.
“In these mice, we are skipping the aggregated proteins, which are usually thought of as the triggers of dementia, and going straight to the downstream effects,” Dr. David Katz,said.
Researchers examined the patterns of gene activity that were changed in the LSD1-deleted mice, they found signs of inflammation and changes in cell metabolism and signaling similar to those seen in Alzheimer’s disease and certain types of FTD.
LSD1’s absence appears to release a combination of several stresses that mirror the stresses on brain cells seen in Alzheimer’s disease and FTD, representing the first time LSD1 has been linked to neurodegenerative diseases.
Researchers say the study may lead to new drug targets for treatment, with compounds that enhance the function of LSD1 or just stop LSD1 from interacting with proteins such as Tau that affect both diseases seen as potentially useful.
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