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First observations of a significant decrease in Alzheimer's disease
Researchers at the Lerner Research Institute in Cleveland have managed to suppress Alzheimer's disease by inhibiting an enzyme in the brain. This raises new hope for Alzheimer's patients that a drug or therapy will be developed in the future that will not only reduce symptoms, but could possibly completely reverse the disease. So far, Alzheimer's dementia has only been reversed in mice. Trials on humans are still pending.
The scientists found that the gradual exhaustion of a certain enzyme in the brain could be the key to remedying the brain disease. There are currently no treatments that can stop the progression of Alzheimer's disease. Around a million people in Germany are affected by the disease and the number is constantly increasing. The study, recently published in the Journal of Experimental Medicine, describes how the inhibition of the enzyme BACE1 can be used to stop the development of dangerous protein deposits in the brain that are involved in triggering the disease.
Alzheimer's disease, also called Alzheimer's disease or Alzheimer's dementia, is an organic brain or neurodegenerative disease in which those affected suffer from a pronounced lack of the brain's memory, language and orientation functions and have impaired thinking and judgment. Many of those affected also experience personality changes due to illness. Most sufferers are over 65 years old.
Alzheimer's disease course
The disease begins with mild dementia, which slowly but steadily worsens and can lead to complete loss of control of many brain and body functions. Alzheimer's disease does not directly lead to patient death, but it increases the susceptibility to infection. Infectious diseases are therefore the most common cause of death in Alzheimer's patients.
Exact causes of the disease are still unclear
The disease was first documented over 100 years ago. However, Alzheimer's has not been fully researched and understood until today. According to current knowledge, researchers suspect that the protein amyloid-beta (beta-amyloid) is a decisive factor in Alzheimer's disease. The protein is suspected to be a trigger and its presence is considered a symptom of the disease. The beta amyloids clump and form insoluble deposits called amyloid plaques. These deposits interfere with the communication of the nerve cells.
The scientists were able to prevent plaque formation
In particular, the scientists were able to successfully reverse the formation of the dangerous amyloid plaques in the brain of the mice, which may also pave the way for similar treatments in humans. The decisive factor was the inhibition of the enzyme BACE1, whereupon the development of amyloid plaques in the brain could be stopped.
The importance of the enzyme BACE1
BACE1 helps produce the harmful plaques by cleaving the amyloid precursor protein into the harmful beta-amyloids. A number of drugs have already been developed as possible therapies that inhibit BACE1 and thus stop the formation of amyloid plaques. The problem, however, is that the enzyme also controls other important cleavage processes. Complete exclusion can seriously affect brain functionality. The team led by the main author of the Riqiang Yan study developed an approach that could prevent BACE1 from forming plaques without affecting the basic functionality of the brain.
Studies of mouse brains provided the clues
The scientists managed to breed mice that decrease the BACE1 enzyme with increasing age. The result was that plaques initially formed in the rodents' brains, but these began to decrease with a falling BACE1 level until the deposits finally disappeared completely. "As far as we know, this is the first observation of such a dramatic reversal of amyloid deposition with every examination of Alzheimer's mouse models," Yan told the magazine "alphr Bioscience".
Side effects of the missing enzyme
However, the results were not entirely positive. Images of the neurons in the mouse brains showed that the functionality of the synapses could only be partially restored, even though the plaques had disappeared. The researchers assume that the BACE1 enzyme is required for information processing in the brain in order to function at an optimal level.
Nevertheless, there is hope for a future Alzheimer's cure
BACE1 functionality appears to be an elusive equilibrium, but there is hope that further testing can be done to determine the ideal levels of the interfering enzyme. If the scientists succeed in future studies in making better use of the BACE1 enzyme, a new form of therapy for Alzheimer's could develop that can not only stop the disease, but also reverse it. (vb)