Alzheimer's causes more diverse than previously thought

The cortex of an animal model of Alzheimer's disease(Credit: Pics56)

Researchers have been discovering more and more about Alzheimer's disease, and some significant progress has been made in bettering our understanding of the degenerative condition. Now researchers from Lund University in Sweden have shed a little more light on the disease, finding that an excessive buildup of amyloid beta isn't solely linked to hereditory factors. The work could lead to more targeted treatment plans for tackling the disease.

Breakthroughs in our understanding of Alzheimer's occur on a seemingly daily basis, with recent studies examining the mechanism by which brain connections are destroyed in the early stages of the disease, looking to non-invasive ultrasound treatments to combat it, and much more. Despite the pace of progress, there's still a huge amount we don't yet understand about the disease. The new study looked specifically at amyloid beta build up, which leads to an accumulation of plaques, inhibiting nerve function and impairing patient memory.

A relatively small percentage of Alzheimer's sufferers have a hereditary risk gene that causes amyloid beta to be overproduced in the brain, directly leading to the condition. In all other cases, the plaque buildup has been attributed to problems with breaking down and remove amyloid beta, rather than the body producing too much of it in the first place. The results of the new study challenge that view, revealing a more complex picture of amyloid beta's role in the condition.

The new study involved 330 people, with one group suffering from a mild cognitive disorder that can be an early sign of Alzheimer's, and a second control group of healthy individuals. Three different methods were used to test participants, with the researchers using a PET scanner, performing genetic analysis and taking cerebrospinal fluid samples.

The results showed an association between an accumulation of amyloid beta in the brain and high levels of specific amyloid peptides in the cerebrospinal fluid. According to the researchers, the link shows that overproduction of amyloid beta, rather than just problems with disposing of it, can contribute to development of Alzheimer's in patients, even if they don't have the hereditary risk gene. In those cases, its thought to be a two stage problem, with the patient producing too much of the protein, while also having problems breaking it down.

That knowledge represents yet another piece of the puzzle, helping us to build a more complete picture of the disease. In the long run, the researchers believe that it could help in the development of new treatments.

"The results are important because they increase the understanding of how Alzheimer's disease arises," said Lund University's Oskar Hansson. "Our hope is that this and other similar studies can increase the possibilities of personalizing treatments that slow down the disease in the future."

The findings of the research were published in the journal Nature.

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