Another cause of Alzheimer's disease?
Scientists from the Langone Medical Center in New York (NYU Langone Medical Center) have identified a new protein-based factor contributing to the development of Alzheimer's disease.
During the formation of beta-amyloid, several more small peptide molecules are split off from its precursor protein (β-amyloid precursor protein, APP). One of them, βCTF (β C-terminal fragment), causes endosome cell dysfunction, which has previously been associated with the death of brain cells in Alzheimer's disease.
The study used cells of patients with Down syndrome, genetically predisposed to the development of Alzheimer's disease due to the fact that the gene encoding the precursor protein beta-amyloid is located on the 21st chromosome, an extra copy of which is the cause of Down syndrome in general. The experiment showed that elevated levels of βCTF, regardless of the concentration of beta-amyloid, cause the same endosome defects and pathological processes in nerve cells as in Alzheimer's disease.
Endosomes are membrane vesicles that support the vital activity of cells by absorbing nutrients from the extracellular space and play a crucial role in maintaining the functions of nerve cells. In Alzheimer's disease, disorders of the structure of endosomes serve as an early sign of the pathological process, appearing first of all in the case when any of the main genetic risk factors are inherited. In addition, scientists suggest that endosomes are the site of amyloid synthesis in cells.
Researchers of Alzheimer's disease, in addition to other problems, are looking for an answer to the question whether beta-amyloid is the only cause of the disease and whether a decrease in its level remains the only hope for recovery. The authors of this work were able to demonstrate that another protein factor, βCTF, is undoubtedly associated with the development of Alzheimer's disease and may be equally important in the development of effective treatment methods.