Personalized clinical managements through exploring circulating neural cells and electroencephalography

BACKGROUND: Since an initial diagnosis of Alzheimer disease (AD) in 1907, early detection, was unavailable through 116 years. Up-regulation of V-Ets erythroblastosis virus E26 oncogene homolog 2 (Ets2) is capable to enhance neuronal susceptibility and degeneration. Protein expression (PE) of Ets2 has functional impact on AD and Down’s syndrome, with diverse intensity. PE of Ets2 has an influential pathogenic impact on AD. Clinical aspects of neurological disorders directly interact with psychological maladies. However, deterioration requires an early management including programmed based protection. AIM: To include cell biology in neuro-genetics; personalized, prognostics, predictive, preventive, predisposing (5xP) platform, accompanied by stratifying brain channels behavior pre- and post-intervention by light music in the AD-patients. METHODS: Include exploration of PE assay and electroencephalography of brain channels. The processes are applied according to: (1) Triangle style, by application of cellular network; and (2) PE assay of Ets2 in the peripheral blood of the patients with AD, by Manual single cell based analysis, and Flow-cytometry. (1) Applying the Genetic counselling and pedigree analysis; (2) considering the psychological status of the referral cases; (3) considering the macro-and/or micro-environmental factors; (4) performing the required Genetics’ analysis; and (5) applying the required complementary test(s). RESULTS: PE of Ets2 has pathogenic role in AD. PE unmasked the nature of heterogeneity/diversity/course of evolution by exploring Ets2, D1853N polymorphism in Ataxia Telangiectasia mutated gene (ATM), vascular endothelial growth factor (VEGF), epidermal growth factor (EGF) and course of evolution at the single cell level of the brain. Ets2 revealed different cellular behavior in the blood and suggested the strategy as ‘Gene Product-Based Therapy’ and the personalized managements for the patients. PE reflected weak expression of ATM, mosaic pattern of Ets2; remarkable expression of VEGF and EGF by highlighting an early detective platform, considering circulating neural cells (CNCs) and the required molecular investigation, for the target individual(s) predisposed to AD or other neural disease including brain neoplasia. Brain channels-cooperation with diverse/interactive-ratios lead to strategic balancing for improving the life-quality in AD. CONCLUSION: We highlighted application of the single CNCs and correlated Ratio based between Brain channels by providing the 5xP personalized clinical management model for an early detection and therapy of the patients with AD and their targeted/predisposed relatives. Novel-evolutionary/hypothetic/heterogenic-results in brain-channels offer personalizd/constructive markers with unlimited cooperation in health and disease.