Dementia arises as a result of brain cell death, which may lead to a decline in learning, memory, and other cognitive functions, but precisely what triggers this process has been unclear. Now, a new study helps to shed some light.
Researchers found that lack of a gene called lysine specific histone demethylase 1 (LSD1) triggers brain cell death, leading to cognitive abnormalities comparable to those seen in people with Alzheimer’s disease and frontotemporal dementia (FTD).
Study co-author David Katz, Ph.D., and colleagues recently reported their findings in the journal Nature Communications.
Alzheimer’s disease is the most common form of dementia, accounting for around 60 to 80 percent of cases. Around 5.5 million adults in the United States have the condition, of whom around 5.3 million are aged 65 and older.
In Alzheimer’s, brain cell death has been partly attributed to a protein called tau. This protein can form “tangles” that interfere with the nerve cells’ transport system, preventing them from receiving the nutrients they need for survival.
FTD is a rarer form of dementia characterized by nerve cell loss in the frontal lobes of the brain. This can lead to personality changes and mobility impairments, as well as problems with language, speaking, and writing skills.
It is estimated that around 50,000 to 60,000 people in the U.S. are living with one of two primary forms of FTD: behavior variant frontotemporal dementia or primary progressive aphasia.
As with Alzheimer’s disease, nerve cell loss in FTD has been attributed, in part, to tau accumulation. The condition has also been linked to the buildup of a protein called TDP43.
The new research from Dr. Katz and colleagues furthers our understanding of the mechanisms underlying nerve cell death in Alzheimer’s disease and FTD, after uncovering a crucial role for LSD1, which is also known as KDM1A.