Researchers find a potential target for anti-Alzheimer treatments

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Scientists at the Luxembourg Centre for Systems Biomedicine (LCSB) of the University of Luxembourg have identified a gene that may provide a new starting point for developing treatments for Alzheimer’s disease (AD). The USP9 gene has an indirect influence on the so-called tau protein, which is believed to play a significant role in the onset of Alzheimer’s disease.

Scientists at the Luxembourg Centre for Systems Biomedicine (LCSB) of the University of Luxembourg have identified a gene that may provide a new starting point for developing treatments for Alzheimer’s disease (AD). The USP9 gene has an indirect influence on the so-called tau protein, which is believed to play a significant role in the onset of Alzheimer’s disease.

This discovery by the LCSB researchers, led by Dr. Enrico Glaab, may open a new door to developing active ingredients to treat Alzheimer’s disease (AD). The scientists recently published their findings in the journal Molecular Neurobiology (DOI: 10.1007/s12035-016-0299-z).

Alzheimer’s disease is characterized by the progressive destruction of brain cells and their contacts (neurons and synapses). The brains of Alzheimer patients exhibit protein deposits known as amyloid plaques. The symptoms of the disease are memory disorders, disorientation, speech impediments, impaired thinking and judgment, and even personality changes. The likelihood of developing AD increases dramatically with age. The number of people affected is, therefore, rising along with our increasing life expectancy: An estimated 35 million people in the world have Alzheimer’s disease today. By 2030, this number could rise to about 65 million, and by 2050 to over 100 million.

It has never been fully explained how the disease develops. It is likely, however, that molecular malformations in brain cells play a crucial role, involving among other molecules the so-called tau proteins. In Alzheimer’s patients, tau proteins aggregate into tangles of threadlike structures, called neurofibrils, which deposit between the brain cells and disrupt their function.

Read more at University of Luxemburg 

illustration: © LCSB / University of Luxembourg