by A new study conducted by researchers at the University of Pittsburgh suggests that the severity of amyloid deposition in the brain, rather than age alone, may be crucial in determining who will benefit most from new anti-amyloid therapies to delay the progression of Alzheimer’s disease. The findings, published in Neurology, reveal that while the accumulation of toxic amyloid beta (A-beta) clumps, which signal Alzheimer’s disease pathology, accelerates with age, the baseline amyloid burden and overall brain health prior to this acceleration are more accurate predictors of progression to Alzheimer’s.
The complexity of increased amyloid accumulation in individuals who are cognitively normal is vital for the improved implementation of dementia treatments, according to corresponding author Dr. Oscar Lopez, a professor of neurology at Pitt and chief of cognitive and behavioral neurology at UPMC.
However, most studies that have measured A-beta burden in the brain using imaging techniques have focused on younger populations, leaving the connection between A-beta and dementia in the oldest individuals unclear.
To address this gap, Lopez and his colleagues examined the relationship between A-beta deposition and new cases of dementia in 94 elderly individuals who were cognitively unimpaired at the start of the study. The participants, with an average age of 85, were followed for 11 years or until their passing, receiving at least two PET scans during the study. The rate of amyloid deposition in their brains was compared to a younger group from the Australian Imaging, Biomarker, and Lifestyle (AIBL) study.
The researchers observed a steady increase in A-beta accumulation in all participants over time, regardless 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, providing an explanation for the higher prevalence of A-beta in the oldest age group.
Only a small number of participants developed dementia without having A-beta deposits in the brain. Importantly, individuals with positive amyloid brain scans at the start of the study developed dementia two years earlier than those who were amyloid-negative.
The study also found that short-term changes in A-beta over a period of 1.8 years could not predict future dementia risk. Instead, the severity of baseline A-beta burden, along with other markers of brain damage such as white matter lesions (indicative of small vessel disease) and a decrease in gray matter thickness in the brain cortex (reflective of neurodegeneration), were the strongest predictors of risk. These findings suggest that an active pathological process was already in place at the onset of the study.
According to Dr. Lopez, the findings align with previous studies suggesting that amyloid accumulation in the brain takes several decades to develop and occurs in conjunction with other brain pathologies, notably small vessel disease. However, the study did not examine the potential parallel vascular process alongside A-beta deposition. Nevertheless, understanding the timing of the presence of these pathologies will be crucial for the implementation of future primary prevention therapies.
The research involved collaboration from various authors, including Dr. Victor Villemagne, Dr. YueFang Chan, Dr. Anne Cohen, Dr. William Klunk, Dr. Chester Mathis, Dr. Tharick Pascoal, Dr. Milos Ikonomovic, Dr. Beth Snitz, Dr. Brian Lopresti, Dr. Ilyas Kamboh, and Dr. Howard Aizenstein, all from the University of Pittsburgh.
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1. Source: Coherent Market Insights, Public sources, Desk research
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