Neuro Receptor Signal Detecting and Monitoring Smart Devices for Biological Changes in Cognitive Health Conditions.

Background: Currently, wearable sensors significantly impact health care through continuous monitoring and event prediction. The types and clinical applications of wearable technology for the prevention of mental illnesses, as well as associated health authority rules, are covered in the current review. Summary: The technologies behind wearable ECG monitors, biosensors, electronic skin patches, neural interfaces, retinal prosthesis, and smart contact lenses were discussed. We described how sensors will examine neuronal impulses using verified machine-learning algorithms running in real-time. These sensors will closely monitor body signals and demonstrate continuous sensing with wireless functionality. The wearable applications in the following medical fields were covered in our review: sleep, neurology, mental health, anxiety, depression, Parkinson's disease, epilepsy, seizures, and schizophrenia. These mental health conditions can cause serious issues, even death. Inflammation brought on by mental health problems can worsen hypothalamic-pituitary-adrenal axis dysfunction and interfere with certain neuroregulatory systems such as the neural peptide Y, serotonergic, and cholinergic systems. Severe depressive disorder symptoms are correlated with elevated Interleukin (IL-6) levels. On the basis of previous and present data collected utilizing a variety of sensory modalities, researchers are currently investigating ways to identify or detect the current mental state. Key message: This review explores the potential of various mental health monitoring technologies. The types and clinical uses of wearable technology, such as ECG monitors, biosensors, electronic skin patches, brain interfaces, retinal prostheses, and smart contact lenses, were covered in the current review will be beneficial for patients with mental health problems like Alzheimer, epilepsy, dementia. The sensors will closely monitor bodily signals with wireless functionality while using machine learning algorithms to analyse neural impulses in real time.

A Review on Neuroinflammatory Pathway Mediating Through Ang-II/AT1 Receptors and a Novel Approach for the Treatment of Cerebral Ischemia in Combination with ARB's and Ceftriaxone.

Background: Ischemic stroke is one of the prevalent neurodegenerative disorders; it is generally characterized by sudden abruption of blood flow due to thromboembolism and vascular abnormalities, eventually impairing the supply of oxygen and nutrients to the brain for its metabolic needs. Oxygen-glucose deprived conditions provoke the release of excessive glutamate, which causes excitotoxicity. Summary: Recent studies suggest that circulatory angiotensin-II (Ang-II) has an imperative role in initiating detrimental events through binding central angiotensin 1 (AT1) receptors. Insufficient energy metabolites and essential ions often lead to oxidative stress during ischemic reperfusion, which leads to the release of proinflammatory mediators such as interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and cytokines like interleukin-18 (IL-18) and interleukin- 1beta (IL-1ß). The transmembrane glutamate transporters, excitatory amino acid transporter-2 (EAAT-2), which express in astroglial cells, have a crucial role in the clearance of glutamate from its releasing site and convert glutamate into glutamine in normal circumstances of brain physiology. Key Message: During cerebral ischemia, an impairment or dysfunction of EAAT-2 attributes the risk of delayed neuronal cell death. Earlier studies evidencing that angiotensin receptor blockers (ARB) attenuate neuroinflammation by inhibiting the Ang-II/AT1 receptor-mediated inflammatory pathway and that ceftriaxone ameliorates the excitotoxicity-induced neuronal deterioration by enhancing the transcription and expression of EAAT-2 via the nuclear transcriptional factor kappa-B (NF-kB) signaling pathway. The present review will briefly discuss the mechanisms involved in Ang-II/AT1-mediated neuroinflammation, ceftriaxone-induced EAAT-2 expression, and the repurposing hypothesis of the novel combination of ARBs and ceftriaxone for the treatment of cerebral ischemia.

Ceftriaxone induces glial EAAT-2 promotor region via NF-kB conformational changes: An interaction analysis using HADDOCK.

Excitotoxicity, depletion of energy metabolites, and ionic imbalance are the major factors involved in neurodegeneration mediated through excitatory amino acid transporter-2 (EAAT-2) dysfunction in ischemic insult. Recent studies have revealed that ceftriaxone expresses EAAT-2 via nuclear transcription factor kappa-B (NF-kB) signaling pathway, stimulation of EAAT-2 expression in the ischemic, and excitotoxic conditions that could provide potential benefits to control neurodegeneration. In this study, we have predicted the in silico model for interaction between NF-kB and EAAT-2 promoter region to rule out the conformational changes for the expression of EAAT-2 protein. Using homology-built model of NF-kB, we identified ceftriaxone-induced conformational changes in gene locus -272 of DNA where NF-kB binding with EAAT-2 promoter region through protein-DNA docking calculation. The interaction profile and conformational dynamics occurred between ceftriaxone predocked and postdocked conformations of NF-kB with DNA employing HADDOCK 2.2 web server followed by 250 ns long all atom explicit solvent molecular dynamics simulations. Both the protein and DNA exhibited modest conformational changes with respect to HADDOCK score, energy terms (desolvation energy [Edesolv ]), van der waal energy (Evdw ), electrostatic energy (Eelec ), restraints energy (Eair ), buried surface area, root mean square deviation, RMSF, radius of gyration, total hydrogen bonds when ceftriaxone pre- and postdocked NF-kB conformations were bound to DNA. Hence, the conformational changes in the C-terminal domain could be the reason for EAAT-2 expression through ceftriaxone specific binding pocket of -272 of DNA.