Although this research started with an interest in inheritance, it unexpectedly led to insights about Alzheimer's disease.
In Alzheimer's, a protein called tau misfolds and accumulates in neurons, especially in the hippocampus, the brain's memory center. When researchers examined the brains of Alzheimer's patients, they discovered something surprising: the LSD1 enzyme was no longer in the , where it should regulate gene expression. Instead, it had become trapped outside the , possibly by tau.
This trapping prevented LSD1 from performing its function, and mimicked the same gene expression changes and neuronal death seen in Alzheimer's.
To test this, researchers engineered Alzheimer's mouse models. Mice lacking LSD1 showed accelerated neurodegeneration, while mice engineered to produce extra LSD1 were protected. These findings suggest that restoring LSD1 activity could potentially slow or prevent the progression of Alzheimer's, a hypothesis currently under study.
If environmental exposures, such as diet, stress, or toxins, can alter gene expression in one generation, should public health policy consider epigenetic inheritance when designing regulations? What ethical questions arise if acquired traits can influence future generations?