Scientists have successfully reversed the symptoms of early Alzheimer's in mice by restoring communication between damaged brain cells. The findings offer an exciting new candidate for future Alzheimer's disease treatments that not only halt the disease in its tracks but may also restore cognitive function.
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Alzheimer's disease affects roughly 5.8 million Americans, according to the Centers for Disease Control and Prevention. The progressive disease is the most common form of dementia and is associated with memory loss and cognitive decline in regions of the brain involved in thought, memory and language.
Today, there is no known cure for Alzheimer's, although scientists believe that it is caused by the abnormal buildup of proteins in and around brain cells. Two main proteins, one of them called tau, have been identified in these abnormal buildups.
Under normal circumstances, tau plays an important role in the chemical communication that allows messages to be transmitted between different brain cells. However, during the early stages of Alzheimer's, this protein begins to detach itself from the network of fibers to which it belongs.
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These free-floating proteins begin to clump themselves together and, in doing so, sweep up other important cellular proteins. Among these important proteins are those involved in sending signals between brain cells.
However, researchers from the Okinawa Institute of Science and Technology Graduate University in Japan have found a way to prevent the tau tangles from sweeping up these important signaling molecules, thus restoring the lost communication between the brain cells.
The treatment involves a synthetic peptide called PHDP5, which the researchers say can easily cross the blood-brain barrier and directly interact with the brain's memory center. After testing their peptide in mice with Alzheimer' s-like symptoms, the team was able to demonstrate PHDP5's restorative capabilities on the early symptoms of Alzheimer's disease. Their results have been published in the journal Brain Research.
"We were thrilled to see that PHDP5 significantly rescued learning and memory deficits in the mice," Chia-Jung Chang, the study's first author, said in a statement. "We successfully reversed the symptoms of Alzheimer's disease in mice."
Chang added: "This success highlights the potential of targeting [this protein] interaction as a therapeutic strategy for Alzheimer's disease."
The team added that the treatment does not "cure" Alzheimer's and still needs to be administered fairly early during the disease's progression, but it does promise to significantly delay symptoms of cognitive decline to a point where they may no longer seriously affect patients within a normal human life span.
The findings come on the same day as a study from the University of Sheffield, published in the journal Nature Communications, revealed new insights into why some people may be more at risk of developing Alzheimer's disease than others.
The second protein involved in Alzheimer's development is called amyloid-beta. Amyloid-beta is produced when proteins in the brain misfold and clump together. These clumps initiate a variety of damaging chemical reactions around our brain cells which damage and eventually destroy them, including the clumping together of tau proteins.
Previous research has demonstrated that a specific version of a gene called APOE significantly increases an individual's risk of developing Alzheimer's, and now, the Sheffield team has demonstrated that this may be because this high-risk variant interacts with amyloid-beta and makes it more damaging to our cells.
The more we can learn about the risk factors associated with this disease, the more effectively we can develop treatments that target different stages of the disease's progression.
Is there a health problem that's worrying you? Do you have a question about Alzheimer's disease? Let us know via health@newsweek.com. We can ask experts for advice, and your story could be featured in Newsweek.
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About the writer
Pandora Dewan is a Senior Science Reporter at Newsweek based in London, UK. Her focus is reporting on science, health ... Read more
