51 results about "Cortical neurons" patented technology

A method of inhibiting the binding between N-methyl-D-aspartate receptors and neuronal proteins in a neuron is disclosed. The method comprises administering to the neuron an effective inhibiting amount of a peptide replacement agent for the NMDA receptor or neuronal protein interaction domain that effect said inhibition of the NMDA receptor—neuronal protein interaction. The method is of value in reducing the damaging effect of injury to mammalian cells. Postsynaptic density-95 protein (PSD-95) couples neuronal N-methyl-D-aspartate receptors (NMDARs) to pathways mediating excitotoxicity, ischemic and traumatic brain damage. This coupling was disrupted by transducing neurons with peptides that bind to modular domains on either side of the PSD-95/NMDAR interaction complex. This treatment attenuated downstream NMDAR signaling without blocking NMDAR activity, protected cultured cortical neurons from excitotoxic insults, dramatically reduced cerebral infarction volume in rats subjected to transient focal cerebral ischemia, and traumatic brain injury (TBI) in rats.

Methods, apparatus and systems for treating sensrineural hearing loss include applying high frequency to ultrasonic frequency vibration stimulus to the head or neck of a patient for a suitable period of time. Hearing and sound discrimination are improved by stimulating the patient's cortices leading to stimulation of cortical neurons to increase sensitivity to high frequency sound. Stimulus signals may be applied by bone conduction via transducers attached to the head or neck, or by airborne conduction via headphones, or by a combination thereof. Stimulus signals may be recorded and may be remotely produced and transmitted via a telecommunications link to a receiver in a remote location. A compact auditory stimulation device includes electronics for storing a personalized stimulus signal, sound generators to produce the stimulus, a microprocessor, and a vibrator, such as headphones. Audiometer functions may be included in the auditory stimulation device to permit testing of the patient's hearing level thresholds.

A method of post-stroke treatment at delayed timepoints with sigma receptor agonists. Sigma receptors are promising targets for neuroprotection following ischemia. One of the key components in the demise of neurons following ischemic injury is the disruption of intracellular calcium homeostasis. The sigma receptor agonist, DTG, was shown to depress [Ca²⁺]_i elevations observed in response to ischemia induced by sodium azide and glucose deprivation. Two sigma receptor antagonists, metaphit and BD-1047, were shown to blunt the ability of DTG to inhibit ischemia-evoked increases in [Ca²⁺]_i. DTG inhibition of ischemia-induced increases in [Ca²⁺]_i was mimicked by the sigma-1 receptor-selective agonists, carbetapentane, (+)-pentazocine and PRE-084, but not by the sigma-2 selective agonist, ibogaine, showing that activation of sigma-1 receptors is responsible for the effects. Activation of sigma receptors can ameliorate [Ca²⁺]_i dysregulation associated with ischemia in cortical neurons, providing neuroprotective properties. The effects of 1,3-di-o-tolyguanidine (DTG), a high affinity sigma receptor agonist, as a potential treatment for decreasing infarct area at delayed time points was further examined in rats. DTG treatment significantly reduced infarct area in both cortical/striatal and cortical/hippocampal regions by >80%, relative to control rats. These findings were confirmed by immunohistochemical experiments using the neuronal marker, mouse anti-neuronal nuclei monoclonal antibody (NeuN), which showed that application of DTG significantly increased the number of viable neurons in these regions. Furthermore, DTG blocked the inflammatory response evoked by MCAO, as indicated by decreases in the number of reactive astrocytes and activated microglia/macrophages detected by immunostaining for glial fibrillary acidic protein (GFAP) and binding of isolectin IB4, respectively. Thus, the sigma receptor-selective agonist, DTG, can enhance neuronal survival when administered 24 hr after an ischemic stroke. In addition, the efficacy of sigma receptors for stroke treatment at delayed time points is likely the result of combined neuroprotective and anti-inflammatory properties of these receptors.

The invention discloses an application of tungstate lithium for preparing a medicine, in particular an application for preparing drug for treating neurodegenerative disease, neuropathy caused by diabetes, and cerebral ischemia including cerebral dysfunction. Both of activity of anion and cation of the tungstate lithium can perform synergistic reaction to inhibit activity of a GSK-3 much better. By inhibiting activity of a GSK-3 alpha, generation of the A beta is reduced to decrease SP; by inhibiting activity of a GSK-3 beta, hyperphosphorylation of tau protein is inhibitted to reduce NFT. Thereby, survival and wound repair of neurocyte are promoted even in a state of ischemia and anoxia to improve learning and memory dysfunction by increasing content of BDNF in cortical neurons.

The invention provides a dyskinesia non-intrusive rehabilitative closed-loop brain-computer integrated system based on an FPGA. The FPGA is used as a control core of the system, nuclei basales and thalamic-cortical prosthesis hardware model is set up, data obtained through calculation of a self-adaptation control algorithm based on the FPGA is used as input to control model parameter setting and force feedback and adjustment until an expected control result is achieved, the self-adaptation control algorithm based on the dynamic causal model is realized, force feedback signals are output, and therefore rehabilitation of patients with the dyskinesia nervous system diseases is achieved. Rehabilitation of the patients with dyskinesia nervous system diseases is achieved, and the complex nuclei basales and thalamic-cortical neuron network and the self-adaptation control algorithm of the dynamic causal model are modeled. The platform provides the effective theoretical basis and technical support for rehabilitation of the dyskinesia nervous system diseases and has important practical value in research on control and treatment on nerve diseases such as Parkinson's disease, epilepsia and alzheimer's disease.

The invention discloses application of a compound tekaning (Chinese character) with a structure in a formula (I) in the specification in preparation of a mitochondrial injury protective agent. In addition, the invention also discloses the mitochondrial injury protective agent of which the effective component is the compound tekaning with the structure in the formula (I). The application fully proves that the compound tekaning, and drugs, drinks or health products containing effective components of the compound tekaning can be used for effectively promoting expression of mitochondrial autophagy key signal molecules, and enhancing mitochondrial autophagy to inhibit the mitochondrial injury, so as to effectively clear mitochondrial dysfunction existing in cortical neuron, especially, dopaminergic neurons of the brain of which the mitochondrial mass is relatively low. Thus, the dopaminergic neuron is protected to play the roles of relieving parkinson's disease and the like and treating a nerve disease.

Human pluripotent stem cells are differentiated in vitro into human cortical spheroids (hCS), which contain astrocytes, as well as cortical progenitors and neurons for use in analysis, screening programs, and the like.

Protein S is a significant neuroprotectant when administered after focal ischemic stroke and prevents hypoxic/re-oxygenation injury. Purified human plasma-derived or recombinant protein S improves motor neurological function after stroke, and reduced brain infarction and edema. Protein S also enhances post-ischemic reperfusion and reduced brain fibrin and neutrophil deposition. Cortical neurons are protected from hypoxia/re-oxygenation-induced apoptosis. Thus, protein S and variants thereof are prototypes of a class of agents for preventing injury of the nervous system. In particular, a disease or other pathological condition (e.g., stroke) may be treated with such agents having one or more protein S activities (e.g., anti-thrombotic and anti-inflammatory activities, direct cellular neuronal protective effects) although the latter activities are not be required.

The invention discloses an application of cholest-4-ene-3,6-dione in preparing a drug for treating or preventing neuron injury. Cholest-4-ene-3,6-dione can relieve hippocampus neuron oxidative stressinjury caused by glutamic acid, cerebellar granule neuron apoptosis injury caused by potassium deprivation and cortical neuron and cerebellar granule neuron oxidative stress injury caused by glutamicacid, also has a function of remarkably reducing infarct volume in an MACO (middle cerebral artery occlusion) model of a stroke rat and has the potential of a neuroprotective agent used for being developed into multiple acting mechanisms. Neurodegenerative diseases such as the Parkinson's disease, the Alzheimer's disease, the tau protein disease, amyotrophic lateral sclerosis and the like as wellas cerebral stroke, cerebral injury and spinal cord injury are all caused by neuron injury, and neuron injury is further aggravated. Cholest-4-ene-3,6-dione has a protection function on neuron injuryand has potential functions in drugs for treating or preventing neuron injury.

The invention belongs to the field of medical technology and relates to a kudzu-vine root daidzein-7, 4'-dioxo acetic acid compound and a preparation method thereof; the compound has the following formula, wherein R1 and R2 can be the same of different and are chosen from H, metal ions, organic cations, basic amino acid cations, C1-C10 alkyl group independently; R3 and R4 can be the same or different and are independently chosen from H or C1-C10 alkyl group; the kudzu-vine root daidzein-7, 4'-dioxo acetic acid compound, and a carrier or excipient which can be acceptable medically are combined to form medicine composite; the compound and the medicine composite has the advantages of cerebral ischemia resistance, oxygen-poor resistance, myocardial ischemia resistance, antagonistic dysmnesia resistance, platelet aggregation resistance and thrombopoiesis resistance and protecting rat cortical neuron damage caused by oxygen deficit.

The presently disclosed subject matter provides for in vitro methods of inducing differentiation of human stem cells into cortical neurons, and cortical neurons generated by such methods. The presently disclosed subject matter also provides for uses of such cortical neurons for treating neurodegenerative CNS disorders.

The invention relates to a neuroprotective agent. The neuroprotective agent comprises a chemical compound having a structure formula shown as follows. The chemical compound having the structure formula can reduce cell calcium influx through a glutamate receptor invertibility inhibiting function, thus protecting cortical neurons from excitatory toxicity initiated by glutamic acid. The neuroprotective agent is extremely effective.

The invention discloses application of heterophyllin B in improving memory and/or preventing the Alzheimer's disease, particularly discloses the memory enhancement function of a radix pseudostellariae aqueous extract, radix pseudostellariae cyclopeptide extract and heterophyllin B for normal mice and the amelioration function on learning and memory dysfunction of dementia mice by injecting Abeta1-42 to the paracele, and discusses the action mechanism of the heterophyllin B. Results show that the radix pseudostellariae aqueous extract, the radix pseudostellariae cyclopeptide extract and the heterophyllin B can significantly enhance the cognitive memory ability of the normal mice and ameliorate the memory impairment of the dementia model mice, the regeneration of cerebral cortex neurites is promoted, and cortical neuron loss and neurite atrophy which are induced by Abeta are prevented; results prompt that the heterophyllin B, a radix pseudostellariae solution and a cyclopeptide extract may reconstruct the neural circuit network by promoting the regeneration of the neurites to play the memory improvement role, and the heterophyllin B can be used for preparing drugs or health foods for preventing and treating the Alzheimer's disease.

The invention belongs to the field of pharmaceuticals and relates to application of totarol serving as a natural product extracted from podocarpus totara to preparation of a drug for preventing and treating ischemic cerebral apoplexy. A result obtained by researching glutamic acid of rat cortex neurons, a hypoxia and hypoglycemia model and a rat middle cerebral artery occlusion experimental model shows that the totarol can be used for reducing neurotoxicity caused by glutamic acid, reducing neuron injury caused by hypoxia and hypoglycemia, improving the activity of glutathione peroxidase in cortical neurons and brain tissues and the activity of superoxide dismutase, reducing the volume of cerebral ischemia infarct caused after cerebral apoplexy and improving the scores of neurological behaviors. The result proves that the totarol has a remarkable neuroprotective effect for ischemic brain tissues and can be used for preparing a drug for preventing and treating ischemic cerebral apoplexy.

The invention relates to a method for detecting cortical neuron axonal growth guidance. The method comprises the following steps: preparing a stamp with a microscopy channel on a mold through polydimentylsiloxane, buckling the stamp on a glass slide for coating poly-L-lysine, adding a solution containing guidance factors and fluorescent molecules from one side of the channel so as to form parallel stripes with equal intervals after entering ducts; and performing neuron cultivation on the glass slide coated with the fluorescent stripe, observing whether newborn axon enters the stripe containing the guidance factors, and computing proportion of the newborn axon and the stripe, statistically analyzing. The method disclosed by the invention is not only in favor of understanding the forming mechanism of the neural circuit in a brain, but also has potential treatment value to the axonal degeneration and axonal injury diseases. On the basis of the method for detecting the cortical neuron axonal growth guidance, a disease model is established, the specificity expression of the secretion factor in the brain in the time and the space is simulated through exogenously giving cell secretion factor, the functional reconstruction of the neutron is induced, and the experimental basis is established for clinical translational medicine for treating above diseases.

The invention relates to the technical field of cell biology and in particular relates to a separation, purification and culture method of naked mole rat cortical neurons. The cortical neurons are separated from cerebral cortices of newly-born naked mole rats and are purified and cultured by comprehensively utilizing a plurality of types of culture mediums, and a reasonable culture method applicable to poikilothermal rodent mammal naked mole rat cortical neurons is explored. The method provided by the invention can be used for simply, conveniently, efficiently and economically obtaining a lot of naked mole rat cortical neurons with normal functional activity, and cells can still keep biological characteristics under an in-vivo state in an in-vitro environment through culture under a low-oxygen condition, so that special physiological functions of the naked mole rat cortical neurons can be conveniently and directly researched in a pure in-vitro cell culture model, and furthermore, an important theoretical basis is provided for exploring a biological mechanism and applying the biological mechanism to clinically relative fields.

The invention discloses application of 4-methoxybenzyl alcohol in preparation of neuroprotective drugs. 4-methoxybenzyl alcohol may reduce injury of primary cortical neurons OGD/Rep of fetal rats and neuron morphological structure injury and increase survival rate of OGD/Rep injured cortex; the release of OGD/Rep injured cortical neuron NO is reduced, activity of SOD (superoxide dismutase) in cells is improved, generation of MDA (methane dicarboxylic aldehyde) is inhibited, apoptosis of nerve cells may be inhibited through significant up-regulation of Bcl-2 protein expression and down-regulation of Bax protein and Caspase-3 protein expression, neuroprotective effect is good, neuroprotective drugs may be produced, and nerve injury is reduced; in addition, the 4-methoxybenzyl alcohol may promote synapse growth of nerve cells, up-regulate synapse growth related proteins, promote repair of the nerve cells and treat nerve injury.

Methods and compositions for modulating the axonal outgrowth of central nervous system neurons are provided. Methods for stimulating the axonal outgrowth of central nervous system neurons following an injury (e.g., stroke, Traumatic Brain Injury, cerebral aneurism, spinal cord injury and the like) and methods for inhibiting the axonal outgrowth of central nervous system neurons in conditions such as epilepsy, e.g., posttraumatic epilepsy, and neuropathic pain syndrome, are also provided. These methods generally involve contacting the central nervous system neurons with a compound that modulates the activity of N-kinase, or analog thereof. The methods and compositions are particularly useful for modulating the axonal outgrowth of mammalian central nervous system neurons, such as mammalian cortical neurons or retinal ganglion cells. Pharmaceutical and packaged formulations that include the compounds of the invention that modulate the activity of N-kinase are also provided.

Evidence indicates dysregulation. of the immunoregulatory molecule CD45 occurs in Alzheimer's disease (AD). Transgenic mice overproducing amyloid-β peptide (Aβ) and deficient in CD45 (PSAPP/CD45⁻/⁻) recapitulate AD neuropathology. Increased cerebral intracellular and extracellular soluble oligomeric and insoluble Aβ, decreased plasma soluble Aβ increased microglial neurotoxic cytokines TNF-α and IL-1β, and neuronal loss were found in PSAPP/CD45⁻/⁻ mice compared with CD45-sufficient PSAPP littermates. After CD45 ablation, in vitro and in vivo studies demonstrate a microglial phenotype whereby microglia phagocytose less Aβ but display proinflammatory properties. This microglial activation occurs with elevated Aβ oligomers and neural injury and loss as determined by decreased ratio of anti-apoptotic Bcl-xL to proapoptotic Bax, increased activated caspase-3, mitochondrial dysfunction, and loss of cortical neurons in PSAPP/CD45⁻/⁻ mice. These data show that deficiency in CD45 activity leads to brain accumulation of neurotoxic Aβ oligomers and validate CD45-mediated microglial clearance of oligomeric Aβ as a novel AD therapeutic target.