Why Some Neurons Die and Not Others in Alzheimer’s Disease
Researchers with the Gladstone Institutes identified molecular clues that help illuminate why some neurons degenerate and die in Alzheimer’s disease, while others don’t. They found that neurons with high levels of the protein apolipoprotein E (apoE) are more sensitive to degeneration, which is linked to apoE’s regulation of the immune-response cells within neurons. ApoE has long been a target of investigation with Alzheimer’s disease, particularly since people carrying the form of apoE called apoE4 are more susceptible to Alzheimer’s disease.
They utilized single-nucleus RNA sequencing, which shows the ways different genes in any specific cell are expressed and converted into RNA. They could then compare individual cells within a cell type, in addition to across different cell types.
The research was published in the journal Nature Neuroscience.
In their research, they found that in both mice and human neurons, high levels of apoE switched on genes in the major histocompatibility complex class-I (MHC-I). This complex is part of a pathway that eliminates surplus synapses during brain development. It may also signal to the immune system that there are damaged neurons and synapses in the adult brain.
“We think that, normally, apoE turns on the expression of MHC-I in a small number of damaged neurons to produce ‘eat me’ signals that mark the neurons for destruction by the immune cells,” said Yadong Huang, senior author of the study. “You don’t want to keep damaged neurons around because they could malfunction and cause problems.”
And in Alzheimer’s disease, they believe this process for removing damaged neurons might become overactivated in a larger number of cells, which can lead to the progressive loss of neurons.
Esophageal Cancers Turn on Ancient Retroviruses Hidden in the Genome
Investigators at Columbia University found that many esophageal cancers switch on ancient viral DNA embedded in our genome from millions of years ago. These bits of ancient retroviruses are called endogenous retroviral elements (ERVs) and their role in cancer is not new. They have degraded over the centuries and can’t produce viruses, but sometimes they are inserted into other genes, where they disrupt their normal activities, or turn on some cancer-causing genes.
They also believe that ERVs might fight cancer if transcribed into strands of RNA. In this study, working with esophageal organoids from mouse tissue, they found a specific cancer-promoting gene in esophageal cancers called SOX2 that stimulates expression of many ERVs, and the accumulation of it can be toxic to cells.
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