How is your competent? doctor measuring this AND ENSURING you have the correct levels? Oh, YOUR DOCTOR IS DOING NOTHING? Welcome to the club of incompetence!
Brain glucose metabolism is primarily measured using Positron Emission Tomography (PET) scans, where a radioactive tracer called fluorodeoxyglucose (FDG) is injected into the bloodstream, allowing researchers to visualize and quantify the brain's glucose uptake in different regions, effectively indicating its metabolic activity
Levels of Brain Glucose Metabolism Protect Against Cognitive Decline
The preservation of brain glucose metabolism may protect against cognitive decline and dementia onset, according to results of a study published in The American Journal of Geriatric Psychiatry.
Although brain atrophy and hypometabolism are markers for neurodegeneration, existing evidence suggests these 2 components of neurodegeneration have unique pathways.
Researchers from Sungkyunkwan University School of Medicine in South Korea sourced data for this study from the Alzheimer`s Disease Neuroimaging Initiative (ADNI) cohort, which has been collecting data since 2003. Individuals with longitudinal cognitive functional measurements and magnetic resonance imaging (MRI), cerebrospinal fluid (CSF) biomarker, and positron emission tomography (PET) data were assessed for cognitive decline on the basis of metabolic resilience (MR) in the brain. Metabolic resilience was defined as the amount of glucose metabolism in the brain that has been conserved given the degree of brain pathology.
The total study population was made up of 848 individuals with a mean age of 72.7. Of these, 47.6% were women. The participants underwent an average of 4.8 cognitive assessments with 807 attending more than two times. Additionally, 386 participants were followed for more than 10 years. The participants were classified as having mild cognitive impairment (MCI; n=454), dementia (n=126), or were cognitively normal (n=268).
Cognitive resilience (CR; β=.05), brain resilience (BR; β=.07), and MR (β=.07) were associated with slower longitudinal cognitive decline (all P<.001).
In the linear mixed model analysis, the models predicting executive function (Akaike Information Criterion [AIC], 5996) and memory (AIC, 3720.1) were better fit with BR, CR, and MR components than CR and MR (AIC, function: 6038.4; memory: 3740.8; both) or BR and MR (AIC, function: 6653.9; memory: 4199.3). All P<.001.
In the interaction model, apolipoprotein E (APOE) interacted with CR (β=.05; P<.001), BR (β=.04; P <.001), and MR (β=.03; P=.002) for the outcome of executive function whereas APOE only interacted with BR for the outcome of memory (β=.03; P=.01). Gender tended to have an interaction effect with MR for the outcome of executive function (β=1.28×10-3; P=.05) and significantly interacted with BR for the outcome of memory (β=.05; P=.015).
In the survival analysis predicting the conversion from MCI to dementia, CR (hazard ratio [HR], 0.49; 95% CI, 0.38-0.64; P<.001), BR (HR, 0.66; 95% CI, 0.55-0.80; P<.001), and MR (HR, 0.53; 95% CI, 0.43-0.66; P<.001) predicted dementia onset. However, the best predictor was CR (C-index, 0.67), followed by MR (C-index, 0.662) and BR (C-index, 0.631). In the additive model, the best predictor (C-index, 0.707) was the model containing all 3 resiliency metrics (HR, 0.64; 95% CI, 0.49-0.84; P<.001).
The study authors concluded, “[O]ur findings suggest that relative preservation of brain glucose metabolism for a given amount of AD pathology is an important feature for predicting future cognitive decline or conversion to dementia.”
This study may have been limited by not using a composite tau measurement incorporating both PET and CSF biomarkers, instead of only defining tau by CSF.
This article originally appeared on Psychiatry Advisor
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