While there’s currently no cure for Alzheimer’s disease, there may be new hope for millions of people worldwide impacted by the cognitive condition. Researchers are one step closer to blocking a protein that plays a key role in the disease, following successful trials on mice.
A research team from Lund University in Sweden believe there’s a clear link between a protein called galectin-3 and Alzheimer’s and found that shutting off the gene decreases inflammation and plaque associated with it.
Alzheimer’s involves the accumulation of amyloid plaques outside cells and a protein called tau which form lumps within nerve cells. When the body’s innate immune defence system discovers these plaques, it triggers the brain’s immune response. Researchers believe the galectin-3 protein plays a major role in this mechanism.
When this inflammatory response continues for long periods it creates a toxic environment which leads to the breakdown and death of nerve cells and the onset of Alzheimer’s disease. The study, published in the Acta Neuropathologica Journal, claimed galectin-3 is required to activate cells that cause plaque formation in the brain.
“We have found that this inflammatory protein increases tenfold in the brains of deceased patients with Alzheimer’s disease, and we especially find it in the microglial cells [which clean out harmful proteins in the brain] that accumulate around the amyloid plaques” researcher Antonio Boza-Serrano said in a statement.
Galectin-3 is involved in inflammation in Parkinson’s disease and after a stroke, but is barely detectable in healthy brains. Researchers believe the effect of the protein can be slowed down by using inhibitors to deactivate galectin-3 during inflammation.
“We grew microglial cells in the lab and added the protein present in Alzheimer’s plaques, which made the cells become very active from an inflammation perspective,” Head of Research Tomas Deierborg said in a statement. “But when we added the galectin-3 inhibitors, the microglial cells became ‘milder’, less inflammatory.”
Mice without galectin-3 performed better during a labyrinth trial, while mice with Alzheimer’s but without the gene that produces the galectin-3 developed less inflammation than mice with it. In fact, mice with Alzheimer’s but without galectin-3 were smarter and had better memory.
“We have shown that by removing galectin-3, we can decrease the amount of plaque and inflammation in the mice, but we have not studied whether this works in humans,” Deierborg said. “There is every reason to continue and to investigate this further.”
Researchers hope the findings can lead to future treatments for Alzheimer’s disease in humans. The disease is caused by the abnormal build-up of proteins in and around brain cells, but little is known about what causes this process to begin. Age, family history, cardiovascular disease and head trauma are some of the biggest known risk factors.
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