NEW DELHI, Dec 23: Overall brain health, not only protein clumping and age, is a more powerful predictor of who is likely to progress to Alzheimer’s disease, a new study has found.
Researchers said that while the clumping of starch-like amyloid proteins in the brain, known to signal Alzheimer’s disease, accelerates in old age, other aspects such as the presence of lesions or a decrease in gray matter thickness are better predictors of the progressive neurodegenerative disease.
“Our findings are consistent with studies showing that the amyloid accumulation in the brain takes decades to develop, and occurs in the context of other brain pathologies, specifically small vessel disease,” said Oscar Lopez, professor of neurology at the University of Pittsburgh, US, and corresponding author of the study published in the journal Neurology.
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In this research, 94 elderly cognitively unimpaired individuals were enrolled at an average age of 85 and followed for 11 years or until their passing. Their rate of protein clumping in the brains was compared to those of a younger group from the Australian Imaging, Biomarker, and Lifestyle (AIBL) study.
The researchers found a steady increase in the clumping of amyloid proteins, or amyloid accumulation, in the participants’ brains with time, a rate that was “significantly faster” in those in their 80s and older than those in their late 60s.
Further, they also found that the individuals whose brain scans showed protein clumps at the start of the study developed dementia two years earlier than those who did not show protein clumps in their scans.
However, through imaging, the team also found that along with amyloid accumulation, there were other indications hinting at “brain damage”.
These indications included the presence of white matter lesions (suggesting small vessel disease) and a decrease in gray matter thickness in the brain cortex (suggesting neurodegeneration), the researchers said.
They said that these signs of brain damage were the “strongest predictors of the risk” of developing Alzheimer’s disease, and indicated that an “active pathological process was already in place when the study began”, at which point, the researchers had deemed the participants to be cognitively unimpaired.
“Understanding the complexity of the increased amyloid accumulation, when individuals are cognitively normal, is critical for improved implementation of dementia treatments,” said Lopez.
The lead researcher said that while this study could not examine the occurrence of a vascular (vessel-related) process in parallel to the protein accumulation, however, “understanding of the timing of the presence of these pathologies will be critical for the implementation of future primary prevention therapies.” (PTI)
