, new research from the University of Cincinnati bolsters a hypothesis that Alzheimer’s disease is caused by a decline in levels of a specific protein.
Alberto Espay, MD, MSc, professor of neurology at the UC College of Medicine and Director and Endowed Chair of the James J. and Joan A. Gardner Family Center for Parkinson’s Disease and Movement Disorders. Credit: Colleen Kelley/UC Brand + Creative Even in this group of patients thought to have the highest risk of Alzheimer’s disease, the scientists observed similar results as the study of the general population.
Espay said it will be essential to ensure that the elevated levels of the protein introduced into the brain do not then turn into amyloid plaques, since the soluble version of the protein is needed for normal function to make an impact in the brain. Espay said he envisions a future with two approaches to treating neurodegenerative diseases: rescue medicine and precision medicine.
'The research found that people can remain cognitively normal regardless of the amount of amyloid plaques in their brains as long as they maintain a baseline level of soluble amyloid-beta in the brain above 270 picograms per milliliter.'
'The research found that people can remain cognitively normal regardless of the amount of amyloid plaques in their brains as long as they maintain a baseline level of soluble amyloid-beta in the brain above 270 picograms per milliliter.'
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