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Wednesday, June 28, 2017

Human enzyme may be key to unraveling Alzheimer's disease stat : Medical News Today

Abnormal protein buildups (shown here) are involved in a number of neurodegenerative conditions, including Alzheimer's disease. For instance, the brains of people with Alzheimer's disease develop aggregates of tau proteins, and those of people with Parkinson's disease develop collections of alpha-synuclein. Using a mouse model of Alzheimer's disease, the team found that CyP40 could reduce the buildup of aggregated tau, making it more soluble. Learn how disrupting protein interaction might slow Alzheimer's disease. Characterized by a slow deterioration of neurons, neurodegenerative conditions gradually degrade emotional, cognitive, and memory functions.



Human enzyme may be key to unraveling Alzheimer's disease
Lysia Forno/Science SourceThe rogue protein behind Parkinson's disease may also protect your gutThe hallmark brain damage in Parkinson's disease is thought to be the work of a misfolded, rogue protein that spreads from brain cell to brain cell like an infection. "This is the first [study] showing that a protein very, very relevant for Parkinson's disease is able to induce an immune response. "This discovery shows us that the [gut's] nervous system can play a key role in both health and disease," Zasloff says. "This type of approach could also in principle alter the whole natural history of the disease," Zasloff says. In four of nine patients—whose intestines had been biopsied before, during, and after the infection—the αS protein appeared only during the infection, but not before.

This human protein may unfurl toxic tangles in Alzheimer's disease


The rogue protein behind Parkinson's disease may also protect your gut
One example in Alzheimer's disease is tau protein, an often overshadowed counterpart to the more heavily studied amyloid beta protein. For example, while the mouse model mimics Alzheimer's disease, the rodents produce a different form of tau, compared to what's found in the human disease. In this study, mice genetically modified to display features of Alzheimer's disease showed fewer tau tangles and improved memory after gene therapy with CyP40. Going further, the scientists repeated this experiment, but replaced tau with one of two other proteins that tangle in neurodegenerative disease: alpha-synuclein in Parkinson's disease and amyloid beta in Alzheimer's disease. To observe this process, they squirted CyP40 protein into a petri dish with tau tangles, and then examined the mixture under an electron microscope.


collected by :Lucy William

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