Valuable breakthrough in Alzheimer's Disease successfully regressed for the first time

First observations of a significant decline in Alzheimer's disease

Researchers at the Lerner Research Institute in Cleveland have managed to push back Alzheimer's disease by blocking an enzyme in the brain. This raises new hope for Alzheimer's patients that in the future, a drug or therapy will be developed that not only reduces the symptoms, but could possibly completely reverse the disease. So far, Alzheimer's disease could only be reversed in mice. Trying on humans are still pending.

Scientists have found that the gradual depletion of a particular enzyme in the brain may be the key to resolving brain disease. There are currently no treatments that can stop the progression of Alzheimer's disease. The disease affects about one million people in Germany and the number is steadily rising. 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 involved in triggering the disease.

The formation of beta-amyloid plaques, which are responsible for the development of Alzheimer's disease in the brain, can be stopped by inhibiting the BACE1 enzyme. (Image: Juan Gärtner / fotolia.com)

Alzheimer's dementia

Alzheimer's disease, also known as Alzheimer's disease or Alzheimer's dementia, is a brain organic or neurodegenerative disease in which sufferers suffer from a marked lack of memory, language and orientation function of the brain and have impaired thinking and judgment. Many people also experience illness-related personality changes. Most sufferers are over 65 years old.

Alzheimer's disease

The disease begins with a mild dementia that is slowly but steadily worsening, leading to complete loss of control of many brain and body functions. Although Alzheimer's disease does not directly lead to the death of the patients, but increasingly increases the susceptibility to infection. Infectious diseases are therefore the leading cause of death in people with Alzheimer's disease.

Exact causes of the disease still unclear

The disease was documented for the first time over 100 years ago. Nevertheless, Alzheimer's is still not fully explored and understood. According to current knowledge, researchers suspect that the protein amyloid-β (beta-amyloid) is a crucial factor in Alzheimer's disease. The protein is suspected as a trigger and its presence is considered a symptom of the disease. The beta-amyloids clump together to form insoluble deposits called amyloid plaques. These deposits disturb the communication of nerve cells.

The scientists were able to prevent plaque formation

In particular, the scientists have been successful in reversing the formation of dangerous amyloid plaques in the mouse brain, possibly paving 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 assists in the production of harmful plaques by cleaving the amyloid precursor protein into the harmful beta-amyloids. Although a number of drugs have been developed as a possible therapy to inhibit BACE1 and thus stop the formation of amyloid plaques. The problem, however, is that the enzyme also controls other important cleavage processes. A complete exclusion can seriously affect the functionality of the brain. Riqiang Yan, the lead author of the study, has developed an approach that could prevent BACE1 from forming plaques without affecting the basic functionality of the brain.

Examinations of mouse brains provided the clues

The scientists managed to breed mice that reduce the BACE1 enzyme with age. The result was that although plaques formed in the brains of rodents, they declined with decreasing BACE1 levels until the deposits finally disappeared altogether. "To our knowledge, this is the first observation of such a dramatic reversal of amyloid deposition in any study of Alzheimer's mouse models," Yan told the magazine "alphr Bioscience.".

Side effects of the missing enzyme

However, the results were not entirely positive. Recordings of the neurons in the mouse brains showed that the functionality of the synapses could only be partially restored although the plaques had disappeared. The researchers assume that the BACE1 enzyme is needed for information processing in the brain to function at optimal levels.

Nevertheless, there is hope for future Alzheimer's healing

The BACE1 functionality appears to be a difficult balance to achieve, but it is hoped that further studies can be performed to determine the ideal levels of interfering enzyme. Should scientists be able to make better use of the BACE1 enzyme in future studies, this could lead to the development of a new form of Alzheimer's therapy that can not only stop but also reverse the disease. (Vb)