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A new study reveals that the amount of amyloid deposition in the brain, rather than just age, may be crucial in determining who will benefit from new anti-amyloid therapies to slow the progression of Alzheimer’s disease.
The accumulation of toxic amyloid beta clumps that signify Alzheimer’s pathology accelerates in old age, but the baseline amyloid burden and the overall brain health at the start of this acceleration are more important indicators of who is most likely to advance to Alzheimer’s, according to University of Pittsburgh clinicians and scientists. The report is published today in Neurology.
Oscar Lopez, M.D., professor of neurology and chief of cognitive and behavioral neurology at UPMC, stated “Understanding the complexity of the increased amyloid accumulation, when individuals are cognitively normal, is critical for improved implementation of dementia treatments.”
Amyloid beta clumps are one of the most prevalent neuropathologies connected with Alzheimer’s. Although people aged 80 and older have the highest prevalence of Alzheimer’s-associated dementias, most research on A-beta burden in the brain has focused on younger individuals. This study aimed to clarify the link between A-beta and dementia in the oldest of the old.
Lopez and his colleagues examined the connection between A-beta deposition and new cases of dementia in 94 elderly individuals who were cognitively unimpaired when the study began. Participants were enrolled in the study at an average age of 85 and followed for 11 years or until their passing, receiving at least two PET scans over the course of the study. The rate of amyloid deposition in the brain of these individuals was compared with a younger group from the Australian Imaging, Biomarker, and Lifestyle (AIBL) study.
Researchers observed a steady increase in A-beta accumulation in all participants over time, independent of their A-beta status at the beginning of the study. However, this accumulation was significantly faster in patients aged 80 and older compared to those in their late 60s, explaining the higher prevalence of A-beta in the oldest of the old.
Ultimately, very few participants developed dementia without having A-beta deposits in the brain. Those with positive amyloid brain scans at the study’s outset developed dementia two years earlier than those who were amyloid-negative.
Researchers also discovered that the short-term change in A-beta alone over 1.8 years could not predict future dementia risk. In contrast, the severity of baseline A-beta burden, as well as other markers of brain damage like white matter lesions and the loss of gray matter thickness in the brain cortex, were the strongest predictors of risk. This suggests that an active pathological process was already in place at the beginning of the study. » …Read More
