Alzheimer’s Breakthrough As Drug Fights Damage in Late-Onset Disease

Scientists have developed a method to “transform” patient skin cells into brain neurons, enabling the study of Alzheimer’s disease without the need for a brain biopsy.

This method has led to the discovery of a drug able to fight the damage in late-onset Alzheimer’s disease.

Researchers at Washington University School of Medicine have successfully grown lab neurons that accurately replicate key features of dementia, such as amyloid beta buildup, tau protein deposits, and neuronal cell death, for the first time.

More From Newsweek Vault: What Is a Health Savings Account?

By studying these skin cells, the researchers identified aspects of the cells’ genomes— called retrotransposable elements, which change their activity as we age—in the development of late-onset Alzheimer’s disease.

“Sporadic, late-onset Alzheimer’s disease is the most common type of Alzheimer’s disease, representing more than 95% of cases,” Andrew Yoo, senior author and professor of developmental biology, said in a statement.

“It has been very difficult to study in the lab due to the complexity of the disease stemming from various risk factors, including aging as an important contributor. Until now, we did not have a way to capture the effects of aging in the cells to study late-onset Alzheimer’s.”

More From Newsweek Vault: Compare the Top Health Savings Account (HSA) Providers

The new method of transforming easily obtained skin cells from living patients directly into neurons allows scientists to study Alzheimer’s effects on the brain without the risk of a brain biopsy, while preserving the age-related characteristics of the neurons.

After transforming skin cells into brain cells, the researchers found that the new neurons can grow in a thin gel layer or self-assemble into small clusters called spheroids, which mimic the 3D environment of the brain.

The scientists then compared neuronal spheroids generated from patients with sporadic, late-onset Alzheimer’s disease, inherited Alzheimer’s disease and healthy individuals of similar ages.

The Alzheimer’s patients’ spheroids rapidly developed amyloid beta deposits and tau tangles between neurons. Genes associated with inflammation were activated, followed by neuronal death, mirroring brain…