Scientists Discover Alzheimer’s Sequence

Alissa Sauer
By Alissa SauerOctober 16, 2017

Researchers know that Alzheimer’s disease creates abnormal levels of certain proteins and causes increased inflammation in the brain. What is still largely unknown, however, is how it works together to trigger Alzheimer’s. Scientists recently conducted a study and discovered a link between the three – essentially a cascading effect.

Learn more about this study and the sequence of events that lead to the disease.

The Alzheimer’s Sequence

Researchers have known that people with Alzheimer’s have a high amount of activated immune cells in their brain along with abnormal deposits of the amyloid beta and tau proteins.

Until now, researchers have not been able to see how this all comes together to set the disease in motion and keep it progressing.

A new study published in the journal Cell Reports – and completed by researchers at the University of North Carolina Chapel Hill (UNC) – found that amyloid beta proteins trigger immune cells and cause inflammation that damages neurons, ultimately leading to “bead-like formations” filled with abnormal tau proteins.

Todd Cohen, Ph.D., assistant professor of neurology at UNC says, “It’s exciting that we were able to observe tau – the major Alzheimer’s protein – inside these beaded structures,” adding that stopping the formation of these beaded structures could help people develop “healthier neurons that are more resistant to Alzheimer’s.” Two additional proteins, MMP-9 and HDCA6, appear to encourage the sequence of events that lead to the formation of these bead structures.

The Clue for a Cure

While the Alzheimer’s epidemic continues, researchers look for a cure or preventative measures to stop the disease before it starts. The study found that a key protein (MMP-9) could trigger the bead formation and lead to a sequence of events that then ultimately lead to Alzheimer’s.

Cohen says that “MMP-9 is an inflammatory protein shown to be elevated in the brains of Alzheimer’s patients.”

The team also identified a second protein, HDCA6, which, when blocked by the team, completely prevented the formation of the beads. Drug developers and testers are currently working on HDAC6 inhibitors and looking into how targeting this protein could disrupt and maybe even treat Alzheimer’s.

The groundbreaking study has sparked more research involving mice to confirm and further understand how amyloid turns to inflammation and then to tau protein.

Cohen says of the new study, “If we can demonstrate this cascade in a wild-type mouse, then we’ll be able to study Alzheimer’s and test therapies in ordinary lab mice without the need for artificial genetic engineering used in traditional Alzheimer’s mouse models.”

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Alissa Sauer

Alissa Sauer

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