2024-07-09 11:00:17
A group of Japanese researchers recently succeeded in reversing the early symptoms of Alzheimer’s disease in mice by restoring communication between damaged brain cells. This breakthrough offers a promising new avenue for futurs treatments of the disease Alzheimer’s disease, not only stopping the progression of the disease, but also restoring certain cognitive functions.
Alzheimer’s disease affects approximately 55 million people worldwide, a figure that is expected to double by 2060 due to the aging of the population. This pathologythe most common form of dementia, causes loss of memory and cognitive decline affecting regions of the brain related to thinking, memory and language. Today, there is no known cure for this disease, although scientists believe it is caused by the abnormal accumulation of proteins in and around brain cells, including a protein called tau. Normally, the tau protein plays a key role in chemical communication between brain cells. However, in the early stages of Alzheimer’s disease, this protein breaks away from the fibers to which it belongs and begins to clump together, capturing other proteins that are essential for transmitting signals between brain cells.
Researchers at the Okinawa Institute of Science and Technology Graduate University in Japan have discovered a way to prevent these tau clumps from trapping signaling molecules, restoring lost communication between brain cells. The treatment uses a synthetic peptide called PHDP5, which can easily cross the blood-brain barrier and interact directly with the brain’s memory center. Tested on mouse presenting symptoms similar to those of Alzheimer’s, PHDP5 has demonstrated its ability to restore cognitive functions affected by the disease. The results of this study were published in Brain Research.
Chia-Jung Chang, first author of the study, said: “We were delighted to see that PHDP5 significantly rescued learning and memory deficits in mice.” He added that this success highlights the potential of targeting theinteraction between proteins like strategy therapeutic for Alzheimer’s disease.
Although this treatment does not “cure” Alzheimer’s disease and must be administered early in the progression of the disease, it promises to significantly delay the symptoms of cognitive decline.
By better understanding the risk factors associated with this disease, scientists hope to develop more effective treatments at different stages of disease progression. The work of OIST researchers represents an important step toward new and promising therapies for Alzheimer’s disease.
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