In the search for the causes and possible cures for Alzheimer’s disease, the role of beta-amyloid plaques has been at the center of several lines of research. By attaching to the outside of neuron cells, the protein deposits disrupt neural communications and eventually cause the cells to die. Because this process may be gradual over years, trying to find early warning signs is important for patients, so that they can be properly diagnosed. In a study released this week, researchers have discovered that memory loss is the key early warning sign of Alzheimer’s and how beta-amyloid presence determines the rate of cognitive decline for patients.
As part of the ongoing Australian Imaging, Biomarker and Lifestyle (AIBL) study, the latest research investigated change in a variety of cognitive functions of volunteers over a 36-month period, using neuroimaging, clinical assessments and the Cogstate test battery of neuropsychological functions.
Started in 2006, the AIBL project, located in Melbourne and Perth, has enrolled more than 1200 people over the age of 60, with each person completing a standardized set of neuroimaging tests and cognitive assessments every 18 months. In addition, data on their medical biomarkers, diet and lifestyle is collected to present a complete picture of their brain’s health.
From the AIBL population, healthy older adults (n = 320), individuals with mild cognitive impairment (MCI) (n = 57) and individuals with Alzheimer’s disease (n = 36) were part of the latest test group, including those with and without beta-amyloid present in their brains.
Healthy older adults who were amyloid negative showed no change in cognitive function over the 36 months being investigated, which was consistent with other AIBL studies. Furthermore, healthy older adults with MCI who were amyloid negative did not show cognitive decline over the 36 months
Among individuals in the Alzheimer’s, MCI, and healthy older adult groups who were amyloid positive, the rate of cognitive decline was equivalent with respect to verbal and visual episodic memory over 36 months. For amyloid positive individuals with MCI, decline also went beyond just memory and included trouble with language, attention, and visuospatial functions. As expected, those with Alzheimer’s demonstrated decline on all memory and non-memory functions. While deficits in memory do not plateau as the severity of the disease increases, there is evidence of decline in non-memory functions such as language.
By focusing on memory issues of older adults, especially those with beta-amyloid present, physicians can watch for early signs of Alzheimer’s.
“These results show for the first time, how beta-amyloid influences the rate of cognitive decline from the very earliest stage of the disease right into clinically classified Alzheimer’s disease,” said Dr. Paul Maruff, co-author of the study, Professor at the Florey Institute for Neuroscience and Mental Health and Chief Science Officer at Cogstate. “It shows how the disease begins almost exclusively as a problem of memory, then once it enters the MCI stage starts to involve other aspects of cognition such as language. Once dementia occurs essentially all aspects of cognition decline. These data also provide for us a sound basis for estimating how big a treatment effect any new drug would require to either forestall, or even stop, amyloid related cognitive decline”.
The study appears in the latest version of the journal Brain.
In the video below, Dennis Selkoe, M.D., of Harvard University, explores the role of beta-amyloid in Alzheimer’s disease and the progress in developing treatments to target beta-amyloid.
Questions or comments? Please contact Dan Peterson