A hallmark of age-related diseases such as Parkinson’s disease, type 2 diabetes, or Alzheimer’s disease is the abnormal clumping of proteins in cells.
A hallmark of age-related diseases such as Parkinson’s disease, type 2 diabetes, or Alzheimer’s disease is the abnormal clumping of proteins in cells. In people with these conditions, these protein clumps can result in irregular deposits known as amyloids that disrupt normal cell behaviors. A Yale pathologist recently discovered that these interactions can be dramatically reduced in type 2 diabetes when small amounts of neighboring proteins are present.
To understand these interactions at the molecular level, assistant professor and lead author Zachary Levine and his collaborators ran a series of simulations that revealed how amyloids form. They found that a unique protein neighbor, normally encountered elsewhere in the cell, was able to stabilize the amyloids found in type 2 diabetes with very high precision. These interactions were then verified in further experiments, suggesting that the body might regulate amyloid diseases using a cocktail of stabilizing proteins.
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