Some brains may have a way to compensate for build-ups of beta-amyloid plaque, a protein linked to Alzheimer’s disease, according to a study published in Nature Neuroscience.
The study involved 22 healthy young adults and 49 older adults who showed no signs of mental decline. Researchers used functional MRI (fMRI) to monitor participants’ brain activity while they memorized pictures of various scenes. After participants were shown the images, they were asked to recall if one of the images matched a written description of a scene. Additionally, they were asked about various details of the images they had memorized.
The brain scans showed that 16 of the older adults had beta-amyloid deposits in their brain; the other 55 participants did not
The group with beta-amyloid deposits generally performed as well as those without deposits. However, researchers noted that as detail and complexity of the memory increased, so did the activity in the brains of those with deposits. Dr. William Jagust, the study’s principal investigator, believes this may indicate that the brain has found a way to compensate for the presence of the Alzheimer’s-associated proteins.
The study results could help explain why some older people who have beta-amyloid deposits do not develop dementia. Previous studies suggest that years of mentally stimulating activity may explain why some older people with beta-amyloid deposits are able to compensate while others are not.
Some brains appear to compensate for the build-up of destructive beta-amyloid plaque, new research suggests.The study, published in Nature Neuroscience, could help explain why some older people who have beta-amyloid deposits do not develop dementia. Using brain imaging technology, known as functional MRI (fMRI), the researchers monitored the participants’ brain activity while they memorized pictures of various scenes.
fMRI scans revealed that those with beta-amyloid buildups showed increased brain activity as detail and complexity of the memory increased, indicating that the brain may compensate for the destructive protein.