Brain and Body

What If We Could Treat Alzheimer’s Before It Began?

December 2, 2015 | Kelly Tatera

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A new discovery could lead to early detection and new prevention methods.

Researchers have known that an early sign of Alzheimer’s disease is the loss of synapses, or the structures that connect neurons in the brain. But now, a team of Australian researchers has discovered how these connections between brain cells are destroyed, which could lead to earlier detection of the disease as well as better prevention methods.

This loss of synapses appears to be one of the very first effects of Alzheimer’s, and occurs long before the actual nerve cells start dying. Basically, if scientists figure out how to halt the progress of the disease at this early stage (it’s associated with very mild cognitive impairment in patients), there may finally be a way to stop Alzheimer’s dead in its tracks.

"Synapses are required for all brain functions, and particularly for learning and forming memories,” study leader Dr Vladimir Sytnyk, of the UNSW School of Biotechnology and Biomolecular Sciences, said in a press release. "We have identified a new molecular mechanism which directly contributes to this synapse loss — a discovery we hope could eventually lead to earlier diagnosis of the disease and new treatments."

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The researchers analyzed post-mortem brain tissue donated from people who had died with and without Alzheimer’s. They looked at a specific molecule, called neural cell adhesion molecule 2 (NCAM2), since the brain protein’s job is to physically connect the membranes of synapses and help stabilize long-term bonds between the synapses and the neurons.

After comparing the two groups of brain tissue, the researchers found that the levels of NCAM2 in the hippocampus — the brain region where most of the damage from Alzheimer’s occurs — were significantly lower in the people who had been diagnosed with the disease before death.

Further, the scientists also revealed in mice studies that NCAM2 was broken down by another protein called beta-amyloid, which is the “main component of the plaques that build up in the brains of people with the disease,” according to the study.

These beta-amyloid protein clumps appear to be one of the main drivers of Alzheimer’s so they’ve been a crucial target for researchers of the disease. Now, the Australian scientists hope that NCAM2 will become a new focus, opening the door for an entirely new approach to Alzheimer’s prevention and treatment.

“Our research shows the loss of synapses is linked to the loss of NCAM2 as a result of the toxic effects of beta-amyloid,” said Dr Sytnyk. “It opens up a new avenue for research on possible treatments that can prevent the destruction of NCAM2 in the brain.”

According to the Alzheimer’s Association, the number of people ages 65 and up with Alzheimer’s disease may nearly triple by 2050, skyrocketing from 5.1 million to a projected 13.8 million. The organization also reports that it’s the only cause of death in the top 10 in America that can’t be prevented, cured, or even slowed.

Due to this breakthrough discovery, perhaps we can expect to see some other major advancements in the prevention and treatment of the disease. With the defeat of Alzheimer’s, maybe old age wouldn’t seem so scary after all.

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