Scientists at UC Berkeley published a new study that provides fresh insight into some brains’ ability to adapt to the buildup of a protein commonly associated with the onset of Alzheimer’s.
The research discovered certain individuals have a neural function that makes up for the presence of the protein, beta-amyloid. This workaround may explain why some people who have beta-amyloid deposits, which are linked to the eventual onset of dementia, do not immediately display signs of abnormal cognition.
The study, published Sunday in Nature Neuroscience, was a joint effort between the Lawrence Berkeley National Lab and campus neuroscience and public health departments. The project was led by Jeremy Elman and Hwamee Oh, research fellows at UC Berkeley’s Jagust Lab.
Previous studies showed a link between higher brain activity and the presence of beta-amyloid deposits, but did not show a definite connection between this activity and better mental performance.
To establish this link, researchers compared two groups of “cognitively normal” adults – 22 young subjects and 49 older subjects, which included 16 adults with detectable beta-amyloid deposits.
Subjects were shown pictures and subsequently asked a series of questions about them to test their memory. The researchers measured the subjects’ brain activity using functional magnetic resonance imaging, technology that measures changes in blood flow. Unlike previous research, the study directly illustrated that increased brain activity in beta-amyloid positive subjects corresponded to the complexity of the memory.
“Their brains aren’t always working harder,” Elman said, “(but) it seems that when their brain works harder it works better.”
Older test subjects who were beta-amyloid negative did not show the same increase in brain activity but had the same level of cognitive function.
The paper is the first to suggest a direct link between higher brain activity and cognitive performance in response to beta-amyloid buildup. This higher brain activity is thought to be the brain’s adaptation to the presence of the protein.
But increased brain activity is also linked to additional production of beta-amyloid, a feedback loop that principal investigator William Jagust, a campus neuroscience professor, calls a potential “vicious cycle” for the brain.
“One of the possibilities is people whose brains are less efficient may end up releasing more amyloid into the brain, and that this increased activity is a compensatory step,” Jagust said.
Elizabeth Edgerly, the chief program officer for the Alzheimer’s Association, an organization working in Alzheimer’s research and care, said the study helps answer “unsolved mysteries.” Still, she said, there is a long way to go.
“You’re like, 300 steps in front of a cure with this research,” she said, citing funding and resource challenges that commonly arise in Alzheimer’s research. “But it would enhance our understanding which may someday help us find more effective treatments.”
Contact Philip Cerles and Tahmina Achekzai at [email protected].