Historically, neurologists and the public have thought that memory loss is a normal part of aging. Then emerged the school of thought that while cognitive impairment was more common in the elderly, it was still not a normal part of aging. Dementia was due to Alzheimer’s Disease (AD) due to an accumulation of Aβ (amyloid -beta proteins) in the brain (as well as due to non-AD causes). One interesting question is whether the accumulation of Aβ (amyloid -beta proteins) often found in older individuals without dementia is simply a benign consequence of aging.
One recent study published in JAMA Neurology provides evidence that the accumulation of amyloid-beta is not a normal part of aging even if there is no overt evidence for dementia. This study tested cognitive performance a median of 10 months before postmortem brain donation in centenarians deemed by patient and caregiver report to be cognitively healthy. Those brains were compared with patients with confirmed AD. Specifically , researchers quantitatively measured Aβ loads in the frontal, parietal, temporal, occipital and hippocampal regions. They compared the Aβ loads with performance on neuropsychological tests measuring memory, fluency, attention and information processing speed, and executive function. The centenarians whose brains showed no or low Aβ load performed significantly better on the cognitive tests as compared with patients whose brains had higher Aβ loads.
These findings suggest that there may be rising Aβ deposition in the brain before dementia becomes clinically evident. Subtle memory loss in the elderly should not be brushed off as a normal part of aging. Therapies aimed at reducing amyloid-beta may be beneficial for older people pre-clinical dementia who have biomarker evidence for amyloid-beta accumulation. With further study, the findings may support to make biomarker testing a routine part of elderly care.
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