New research may help scientists make huge strides in their fight against Alzheimer’s disease. This horrific condition is incurable and cannot be stopped at this time. The main cause of the disease is the loss of brain cells and neurons in the brain. This natural degeneration is what forces memory loss and the loss of cognitive functions.
Researchers have not been able to tell which proteins or genes are expressed by certain neurons, even though they can figure out which neurons are the first to die. This is a critical piece of the puzzle because it’s important to identify and recognize changes in certain cells.
A study shows that neurons with a specific protein may be more vulnerable to breaking down in the brain. This is critical because knowing why these neurons are vulnerable could lead to possible treatments.
Now, a recent study has shown that neurons expressing a specific protein are more vulnerable to degeneration. Understanding which neurons are more vulnerable – and why – might allow researchers to develop targets for potential treatments in the future.
Scientists studied the post-mortem brains of those with Alzheimer’s disease for this study. They started to look at the tau protein build-ups in various areas of the brain. Tau proteins aggregate in cells of people with Alzheimer’s disease. This then causes the cell to die off. Different areas of the brain often show differing degrees of degeneration due to the different levels of tau proteins.
After the scientists figured out the progression of the disease, they started to look into the superior frontal gyrus and entorhinal cortex brain regions. These two parts of the brain focus on memory and self-awareness. The entorhinal cortex showed that tau accumulated in the earlier stages of the disease, yet it wouldn’t show up until the later stages in the other area. Scientists were able to investigate the differences in the same cell types in these two different areas of the brain in different stages of the disease.
Researchers were able to find that excitatory neurons were the most vulnerable cells of those researched. This type of neuron generates action signals. The excitatory neurons showed almost a 50% decline during the early stages of the disease. These neurons also on a molecular level contained higher levels of retinoid-related orphan receptor beta. This is interesting because it wasn’t a protein detected in other cells researched, meaning the proteins and genes that a cell express may boost the vulnerability of the cells. RORB may be able to activate or deactivate pathways in the brain that lead to the disease because it helps develop neurons. It’s also able to control a level of proteins in some cells.
Scientists then took other excitatory neurons and RORB-vulnerable excitatory neurons to compare their differences. They found that the neurons involved in sending and receiving signals in the brain and that send messages in the brain had differences in their genes. This would help the scientists confirm that the RORB neurons were more vulnerable to the disease.
The researchers moved to the superior frontal gyrus’ neurons. These neurons seemed to very similar and vulnerable with high levels of RORB. This could mean that high levels of RORB are found in all of the disease stages and in all areas of the infected brain.
Astrocytes regulate neuron activity and protect the brain from infection and disease. Scientists determined that these changed during the disease’s progression. When these were more activated, Alzheimer’s was more progressed in the brain.
This research did not study the brains of women with Alzheimer’s disease. It simply did the study on the different neurons to determine which were more vulnerable to the disease. This is a large step in finding out why different cells are more vulnerable to Alzheimer’s disease. Studying RORB in neurons will continue to produce more results and more questions leading to research that might save lives.
