Researchers indicate that neural compensation among individuals with Alzheimer’s-related protein, a new study shows. The findings from the study, led by UC Berkeley researchers, were published September 14 in the journal Nature Neuroscience.

The recent findings could offer an explanation as to why some older adults with deposits of beta-amyloid, a destructive protein linked to Alzheimer’s, could continue to have normal cognitive function while others develop dementia.

In prior studies, the link between beta-amyloid deposits and brain activity is clear, while any link between the activity and enhanced mental performance remained unclear.

The study’s principal investigator, Dr. William Jagust, a professor with joint appointments at UC Berkeley’s Helen Wills Neuroscience Institute, the School of Public Health and Lawrence Berkeley National Laboratory, said in a statement, “This study provides evidence that there is plasticity or compensation ability in the aging brain that appears to be beneficial, even in the face of beta-amyloid accumulation.”

The study consisted of 22 healthy young adults and 49 older adults without signs of mental decline. Brain scans among the study participants revealed that 16 of the older subjects had beta-amyloid deposits, unlike the remaining 55 adults.

Jagust noted, “Generally, the groups performed equally well in the tasks, but it turned out that for people with beta-amyloid deposits in the brain, the more detailed and complex their memory, the more brain activity there was.” He continued, “It seems that their brain has found a way to compensate for the presence of the proteins associated with Alzheimer’s.”

According to the Alzheimer’s Association, over 5 million Americans live with the disease, which is the sixth leading cause of death in the U.S.