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Neuroplasticity refers to the brain’s ability to change throughout life. This process can be defined as the potential of the neurons to react to intrinsic or extrinsic inputs and to change, temporarily or permanently, their biochemical, physiological and morphological characteristics. The nervous system is capable of adapting to new developmental and environmental situations or neuropathological stress by using pre-existing cognitive processing approaches or by enlisting compensatory mechanisms.
Studies have shown that neuroplasticity might come into play before the onset of Alzheimer’s disease (AD). This skill allows the brain to compensate for the decline in cognitive function and may help delay the symptoms of AD. Deeper understanding of how cerebral glucose metabolism changes during AD has grown rapidly over the past decades. It is known that diminished cerebral glucose metabolism (hypometabolism) occurs early in AD, particularly in people at genetic risk of developing the disease, and correlates with higher amyloid plaque density and lower cognitive scores.
Researchers from Imperial College London investigated glucose metabolism and its relation to amyloid deposition in patients with mild cognitive impairment (MCI), who have an increased risk of developing Alzheimer’s or another dementia. The investigators’ aim was to understand whether increased glucose metabolism (hypermetabolism) may be considered a compensatory mechanism in response to the failure of neurons, before amyloid deposition takes place in AD patients.
MCI subjects underwent [11C]PIB and [18F]FDG PET scans. The imaging tracers that were used allowed the detection of amyloid plaques and the measure of the regional cerebral glucose metabolism, respectively. [11C]PIB and [18F]FDG images of all individuals were sampled in the same regions of interest using Analyze software. Amyloid load and glucose metabolism were assessed by localization of clusters of significant differences in mean compared with images obtained from control subjects.
The investigators found that five out of ten MCI subjects showed hypermetabolism, which was predominantly seen in the occipital cortex, and were also amyloid-negative. The other MCI individuals showed hypometabolism with high amyloid load and converted to AD during clinical follow-up. Hypermetabolism may represent a compensatory response to the neuronal damage occurring early on in the disease process and may predate amyloid deposition in MCI subjects. Once sufficient amyloid has accumulated to exhaust the capacity of the neural networks, hypermetabolism shifts to hypometabolism in the face of increasing metabolic demands of the degenerating neurons.
This particular retained ability of the brain to adapt to neurodegenerative diseases in the attempt to maintain function may provide a valuable opportunity for intervention. These findings infact reinforce the belief that there may be a therapeutic window of opportunity in MCI subjects and people with early-stage AD.
Tags: Alzheimer's Disease, Brain Metabolism, Dementia