Amyloid plaques comprising the beta-amyloid protein can effectively catalyze neurotransmitter degradation, according to a new study by BGU scientists. While amyloid plaques are the hallmark of Alzheimer’s Disease and other neurodegenerative diseases, it is still not clear if, and how, such plaques contribute to disease progression and its pathological implications. This study offers an alternative explanation of how the plaques “poison” the brain by breaking up important neurotransmitters such as dopamine and adrenaline.

The study’s findings were just published in the prestigious peer-reviewed Chem Catalysis, a Cell Press journal.

The research was led by Prof. Raz Jelinek and Ph.D. student Elad Arad, in collaboration with Prof. Hanna Rapaport and Avigail Baruch Leshem. The researchers discovered remarkable catalytic activity that was directly caused by beta-amyloid fibrils, not non-fibril organizations of the protein (smaller protein units such as monomers or oligomers). Importantly, neurotransmitter degradation has been observed in the brains of Alzheimer’s disease patients, suggesting that the fibril-catalysis phenomenon discovered by Jelinek and colleagues may indeed be physiologically significant.

“Our findings open intriguing new avenues of research into the molecular factors in neurodegenerative diseases that could bring us closer to therapeutic treatments,” says Prof. Jelinek.

Prof. Raz Jelinek is the Vice President and Dean of Research & Development at BGU. He and his student Elad Arad are at the Department of Chemistry and the Ilse Katz Institute for Nanoscale Science and Technology (IKI). Prof. Hanna Rapaport is at the Avram and Stella Goldstein-Goren Department of Biotechnology Engineering and IKI. Avigail Baruch Leshem is a member of the Unit of Environmental Engineering.

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