Harvard scientists have made a breakthrough in studying early onset Alzheimer’s Disease by converting patients’ skin cells into neurons in the hopes of facilitating a better understanding of the disease and creation of drug therapies.
The study, led by Tracy Young-Pearse, a Harvard Stem Cell Institute affiliate and member of Brigham and Women’s hospital, concluded what had previously only been observed in mice—that the early onset of Alzheimer’s is directly correlated to higher levels of amyloid beta protein 42. Most people generally produce amyloid beta with only 40 amino acids, but in early onset of the disease, amyloid beta protein 42, which has two extra amino acids, was more prevalent.
As a form of progressive dementia that affects more than 26 million people worldwide, early onset AD usually brings about cognitive decline and memory loss in individuals in their 30’s to 50’s while the more common late onset AD tends to affect individuals in their 70’s, 80’s and 90’s.
Researchers also concluded that the neurons had higher amounts of tau protein, a classic signal of Alzheimer’s presence.
The recent findings could lead to the development of potential therapies for this common disease.
“The ability to direct stem cells generated from patients to become brain cells allows us with an unprecedented opportunity to study, on a large scale, living patient-derived brain cells in a dish,” Young-Pearse said. “Not only can we use these to better understand the mechanisms underlying the disease, but we also can use these to test novel therapeutic strategies in the cell types involved in the disease.”
Moreover, this research serves as a proof-of-concept that stem cells can be used to model diseases and discover therapies.
“The field is highly collaborative, working together to…[make] different types of neurons that are affected in various neurodegenerative diseases including Parkinson's, ALS, Huntington's and Alzheimer's disease,” Young-Pearse said.
—Staff writer Arjun S. Byju can be reached at firstname.lastname@example.org.