|dc.description.abstract||Acquired brain neuronal injury is one of the most significant healthcare problems nationally and globally. Acquired brain neuronal injury results from hypoxemia, biotoxin or ribotoxin exposure, or pressure shifts in the brain neuronal architecture and is responsible for 45% of 42 million dementia cases globally. Biological changes in the brain start decades before cognitive impairment is identified and may be delayed or reversible. In a retrospective study using secondary data analysis, we examined the interrelationships among proteomic biomarkers transforming growth factor-beta1 (TGFβ1), vascular endothelial growth factor (VEGF), matrix metalloproteinase-9 (MMP-9), and complement C4a, and NeuroQuant® data with symptoms of subjective cognitive impairment (SCI) in 30 to 59 years old adults.
As an exploratory analysis not previously investigated for NeuroQuant® data, 195 female and 55 males NeuroQuant® data sets were extracted. There were multiple correlations among upregulated C4a, TGFb1, and VEGF and the intracranial volume (IVC) to the forebrain, cortical grey, ventricles, hippocampus, pallidum, thalamus, caudate, and amygdala. Adults with self-reported poor memory demonstrated volumetric atrophy to the hippocampus, cortical grey, and cerebellum. There were insufficient aged-matched controls to examine the relationship between sociodemographic data, proteomic biomarkers, and NeuroQuant® data in adults.
Peripheral biomarkers C4a, TGFb1, and VEGF are potential indicators of brain parenchymal changes in adults with SCI. Our data suggest pathologies associated with neuronal injury are present in the brain and plasma in adults with SCI. Early screening for acquired brain neuronal injury is essential to allow prompt interventions and prevent SCI progression to mild cognitive impairment (MCI). Routine screening for brain neuronal injury should begin early in primary care and not solely focus on poor memory as an indicator of cognitive impairment. SCI should be investigated further with proteomics, NeuroQuant® examination, and lifestyle alterations.
Future research should include examining chromosomal sex differences in brain neuronal injury, the impact of the female brain's perimenopausal transition to develop a comprehensive understanding of the dynamic metabolic aging process, potential interventions, and possible window of prevention for brain neuronal injury. Additionally, scholarship should investigate molecular hypometabolism and aged-matched controls for NeuroQuant® data, age, and gender.||