Abnormally configured proteins were found to accelerate breakup of the brain’s neurotransmitters.
Abnormally configured proteins known as myloid plaques may cause Alzheimer’s disease by accelerating the breakup of neurotransmitters, Ben-Gurion University scientists have found. It is the first study to show that amyloid fibrils made of the well-known “beta-amyloid” protein catalyze neurotransmitter degradation.
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. The BGU study offers an alternative explanation of how the plaques “poison” the brain by breaking up important neurotransmitters such as dopamine and adrenaline.
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.
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,” said Jelinek, the Vice President and Dean of Research & Development at BGU.
An estimated 50 million worldwide suffer from Alzheimer’s.
World Israel News contributed to this report.