This is the kind of study that’s out of my league of understanding, I have to admit. But it doesn’t make the work less fascinating:

While studying how memories are formed and stored in the brain, a team identified a novel protein folding mechanism that is essential for long term memory storage. The researchers further demonstrated that this mechanism is impaired in a tau-based mouse model of Alzheimer’s disease and that restoring this protein folding mechanism reverses memory impairment in this mouse model for the study of dementia.

We’re still a very long, long way of finding even the beginning of a possible cure and no, you can’t do anything with this insight in your classroom. Still, I’m hooked.

Abstract of the study by Snehajyoti Chatterjee and colleagues, published in Science Advances:

The mechanisms underlying memory loss associated with Alzheimer’s disease and related dementias (ADRD) remain unclear, and no effective treatments exist. Fundamental studies have shown that a set of transcriptional regulatory proteins of the nuclear receptor 4a (Nr4a) family serve as molecular switches for long-term memory. Here, we show that Nr4a proteins regulate the transcription of genes encoding chaperones that localize to the endoplasmic reticulum (ER). These chaperones fold and traffic plasticity-related proteins to the cell surface during long-lasting forms of synaptic plasticity and memory. Dysregulation of Nr4a transcription factors and ER chaperones is linked to ADRD, and overexpressing Nr4a1 or the chaperone Hspa5 ameliorates long-term memory deficits in a tau-based mouse model of ADRD, pointing toward innovative therapeutic approaches for treating memory loss. Our findings establish a unique molecular concept underlying long-term memory and provide insights into the mechanistic basis of cognitive deficits in dementia.