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Scientists have discovered a protein that causes Alzheimer's disease

 
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Last reviewed: 30.06.2025
 
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25 May 2011, 22:46

An enzyme that is involved in regulating cell division and is the cause of some cancers can cause the death of neurons in the brain.

Long-term research by researchers from the Feinstein Institute for Medical Research (USA), specializing in Alzheimer's disease, led them to the c-Abl protein, which scientists believe is one of the main causes of this severe neurodegenerative disease.

C-Abl belongs to the class of tyrosine kinase enzymes, i.e. it attaches a phosphoric acid residue to the amino acid residues of tyrosine in the polypeptide chains of other proteins. The operation increases or decreases the activity of the modified protein. c-Abl is involved in the processes of cell differentiation, cell division and cell adhesion during cell formation. Participation in cell division processes makes c-Abl one of the potential "provocateurs" of cancer. It was previously known that an increase in the level of this enzyme in B-lymphocytes accompanies chronic myeloid leukemia, and if its activity is suppressed, this will slow down the division of cancer cells.

Researchers from the Feinstein Institute were looking for enzymes that phosphorylate the tau protein, which forms characteristic neurofibrillary tangles in neurons of the brain in Alzheimer's disease. The article, announced on the website of the Journal of Alzheimer's Disease, reports that it was the kinase c-Abl that accompanied Alzheimer's plaques and neurofibrillary tangles in the brain. In experiments, this enzyme triggered the cell cycle, pushed neurons to begin dividing, and thereby caused their death. The researchers increased c-Abl activity in the hippocampus and neocortex of mice - and soon discovered the typical "holes" in brain tissue for this disease, which developed most quickly in the hippocampus; the death of neurons was accompanied by intense inflammation.

The laboratory mouse model that the researchers developed for their experiments could serve as a convenient testing ground for creating anti-Alzheimer drugs. The drugs that suppressed c-Abl activity in blood cancer are not suitable for treating Alzheimer's disease: they will not be able to overcome the blood-brain barrier that exists between the circulatory system and the nervous system.

Scientists are now working to clarify the mechanism of cell death caused by this enzyme in order to develop a targeted method of influencing neurons containing the out-of-control protein.

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