62 results about "Synapsis" patented technology

In Pavlovian and instrumental conditioning, rewards typically come seconds after reward-triggering actions, creating an explanatory conundrum known as the distal reward problem or the credit assignment problem. How does the brain know what firing patterns of what neurons are responsible for the reward if (1) the firing patterns are no longer there when the reward arrives and (2) most neurons and synapses are active during the waiting period to the reward? A model network and computer simulation of cortical spiking neurons with spike-timing-dependent plasticity (STDP) modulated by dopamine (DA) is disclosed to answer this question. STDP is triggered by nearly-coincident firing patterns of a presynaptic neuron and a postsynaptic neuron on a millisecond time scale, with slow kinetics of subsequent synaptic plasticity being sensitive to changes in the extracellular dopamine DA concentration during the critical period of a few seconds after the nearly-coincident firing patterns. Random neuronal firings during the waiting period leading to the reward do not affect STDP, and hence make the neural network insensitive to this ongoing random firing activity. The importance of precise firing patterns in brain dynamics and the use of a global diffusive reinforcement signal in the form of extracellular dopamine DA can selectively influence the right synapses at the right time.

This invention describes the administration of multiple therapeutic agents with insulin in conjunction with bexarotene, ketamine, monoclonal antibodies Etanercept, IGF-1, and acetylcholine esterase inhibitors physostigmine, for treatment of Alzheimer's disease and other neurodegenerative diseases. Insulin, improves memory; also augments and amplifies the effects of the adjuvant therapeutic agents (paracrine and intracrine effects) and consequently reduces the β amyloid, its soluble precursors, prevents damage to the neuronal skeletal network (taupathy), and blocks glutamate excitotoxicity, reduces brain inflammation, prevents apoptosis, and increases the acetylcholine levels in the neurons and synapses; by using a combination of insulin, bexarotene, ketamine, Etanercept, IGF-1, and physostigmine therapeutic agents. The results are achieved by using the specially designed Iontophoresis incorporated olfactory mucosal delivery (ORE) catheter device located at the olfactory nerves, sphenoid sinus, and adjacent structures described here, to transport the large molecules of therapeutic agents to treat AD delivered to the CNS bypassing BBB from ORE.

The invention discloses a unit, a device and a method for simulating biological neuron and neuronal synapsis on the basis of chalcogenide compounds. The unit comprises a first electrode layer, a function material layer and a second electrode layer. During the neuron simulation, a device receives the stimulation of one or a plurality of electric pulses, the resistance of the function material is changed into the low resistance state from the high resistance state, the simulated neuron is changed into an excitation state from a resting state, and the threshold value excitation and energy accumulation excitation functions are realized. During the neuronal synapsis simulation, the electric conductance of the function material layer of the device can be gradually changed according to input signals, and the synapsis weight regulating function is realized, the ynapsis weight is changed according to time differences of signals input at two ends, and the STDP (spike timing dependent plasticity) function of synapsis is realized. The basic device forming the artificial neural network can be provided.

The invention discloses a unit, a device and a method for simulating biological neuronal synapsis on the basis of chalcogenide compounds. The unit comprises a first electrode layer, a function material layer and a second electrode layer, wherein the first electrode layer receives first pulse signals, and the second electrode layer receives second pulse signals. A device can change electric conductance simulation synapsis weight changes according to input signals. When the difference value between the frequency of the first pulse signals and the frequency of the second pulse signals is plus or minus, the electric conductance is changed , and the simulation of the pulse frequency dependent synaptic plasticity function of the biological neuronal synapsis is realized. When the signal difference peak value between the first pulse signals and the second pulse signals is plus or minus, the electric conductance is changed, and the simulation of the pulse time dependent synaptic plasticity function of the biological neuronal synapsis is realized. The unit, the device and the method have the advantages that the basic function of the biological neuronal synapsis can be realized on single inorganic devices, the basic device forming the artificial neural network can be provided, and the effects of integration degree improvement and power consumption reduction can be obtained.

The invention discloses a chimeric antigen receptor, a coding gene, an expression vector and application thereof. The chimeric antigen receptor comprises a single chain variable fragment, a CD8 alpha transmembrane domain, a CD3 zeta intracellular signal domain, a first co-stimulator ligand and a second co-stimulator ligand which are in successive tandem connection, wherein the CD8 alpha transmembrane domain is used for connecting the single chain variable fragment to a cell membrane, 2A short peptide is arranged between and in tandem connection with the CD3 zeta intracellular signal domain and the first co-stimulator ligand, and another 2A short peptide is arranged between and in tandem connection with the first co-stimulator ligand and the second co-stimulator ligand. According to the chimeric antigen receptor provided by the invention, the 2A short peptide is used to connect the chimeric antigen receptor with the two co-stimulator ligands, so the two co-stimulator ligands are expressed on the surface of an immune cell at the same time; once the chimeric antigen receptor specifically binds with antigen, the two co-stimulator ligands rapidly migrate to synapses formed by the combination of cells, so activity of immune cells is effectively enhanced.

The invention provides compositions and methods for treating, preventing, and diagnosing diseases or conditions associated with an abnormal level or activity of biglycan; disorders associated with an unstable cytoplasmic membrane, due, e.g., to an unstable dystrophin associated protein complex (DAPC); disorders associated with abnormal synapses or neuromuscular junctions, including those resulting from an abnormal MuSK activation or acetylcholine receptor (AChR) aggregation. Examples of diseases include muscular dystrophies, such as Duchenne's Muscular Dystrophy, Becker's Muscular Dystrophy, neuromuscular disorders and neurological disorders.

A expandable neural network with on-chip back propagation learning is provided in the present invention. The expandable neural network comprises at least one neuron array containing a plurality of neurons, at least one synapse array containing a plurality of synapses, and an error generator array containing a plurality of error generator. An improved Gilbert multiplier is provided in each synapse where the output is a single-ended current. The synapse array receives a voltage input and generates a summed current output and a summed neuron error. The summed current output is sent to the input of the neuron array where the input current is transformed into a plurality of voltage output. These voltage output are sent to the error generator array for generating a weight error according to a control signal and a port signal.

A neuromorphic synapse (11) comprises a resistive memory cell (15) connected in circuitry having first and second input terminals (21,22).These input terminals (21,22) respectively receive pre-neuron and post-neuron action signals, each having a read portion and a write portion, in use. The circuitry also has an output terminal (23) for providing a synaptic output signal which is dependent on resistance of the memory cell (15).The circuitry is operable such that the synaptic output signal is provided at the output terminal (23) in response to application at the first input terminal (21) of the read portion of the pre-neuron action signal,and such that a programming signal,for programming resistance of the memory cell (15), is applied to the cell (15) in response to simultaneous application of the write portions of the pre-neuron and post-neuron action signals at the first and second input terminals (21,22) respectively. The synapse (11) can be adapted for operation with identical pre-neuron and post-neuron action signals.

The invention discloses an inorganic-organic/inorganic hybrid dual-layer nano-film memristor for simulating nerve synapses, and belongs to the cross field of semiconductor microelectronic devices andartificial intelligence. A molecular layer deposition technology and an atomic layer deposition technology are utilized to prepare the inorganic-organic/inorganic hybrid dual-layer nano-film memristorwith a good nerve synapse simulation bionic function; and the adopted molecular layer deposition and atomic layer deposition technologies can be compatible with a microelectronic process and are suitable for large-scale integration. The memristor comprises a substrate, a bottom electrode, a memristor functional layer and a top electrode in sequence from bottom to top, wherein the memristor functional layer consists of two layers of nano-stack structure film materials including a lower-layer inorganic-organic hybrid film and an upper-layer metal oxide film.

Soluble proteins, e.g. thrombospondins, can trigger synapse formation. Such proteins are synthesized in vitro and in vivo by astrocytes, which therefore have a role in synaptogenesis. These thrombospondins are only expressed in the normal brain exactly during the period of developmental synaptogenesis, being off in embryonic brain and adult brain but on at high levels in postnatal brain. Methods are provided for protecting or treating an individual suffering from adverse effects of deficits in synaptogenesis, or from undesirably active synaptogenesis. These findings have broad implications for a variety of clinical conditions, including traumatic brain injury, epilepsy, and other conditions where synapses fail to form or form inappropriately. Synaptogenesis is enhanced by contacting neurons with agents that are specific agonists or antagonists of thrombospondins. Conversely, synaptogenesis is inhibited by contacting neurons with inhibitors or antagonists of thrombospondins.

A neuromorphic device may include: a pre-synaptic neuron; a plurality of post-synaptic neurons; and a plurality of synapses electrically connected to the pre-synaptic neuron and electrically connected to the plurality of post-synaptic neurons. Each of the post-synaptic neurons may include: an integrator; a main comparator having a first input port connected to an output port of the integrator; and a first sub comparator having a first input port connected to the output port of the integrator.

A method for unsupervised learning of a multilevel hierarchical network of artificial neurons wherein each neuron is interconnected with artificial synapses to neurons of a lower hierarchical level and to neurons of an upper hierarchical level. The method includes at a neuron the steps of integrating inference spikes from the interconnected neurons of the lower hierarchical level both in a first and a second accumulators using the same synaptic weights; when the first accumulator reaches a first threshold, generating a learning spike, resetting the first accumulator, triggering synaptic conductance modification in accordance with a spike-timing dependent plasticity rule and delivering the learning spike as an inhibitory signal to other neurons in the same hierarchical level; when the second accumulator reaches a second threshold, generating an inference spike, delivering the generated inference spike to the interconnected neurons of the upper hierarchical level, resetting the second accumulator and possibly delivering the inference spike as an inhibitory signal to other neurons in the same hierarchical level.

The invention relates to the cell transdifferentiation technology in the field of cell research, in particular to a method for inducing neuroblastoma cells to be differentiated to nerve cells. The neuroblastoma cells are cultured for 3-7 days through an inducing culture medium, and then the nerve cells are obtained; the inducing culture medium is obtained by adding retinoic acid to a neural stem cell condition culture solution to 10 micrometers; a complete culture medium including a DMEM/F12 basic cukture mediam, B27, bFGF, EGF, heparn sodium, L-glutamine and mycillin is used for culturing the neural stem cells, the complete culture medium is replaced by a half after culturing is conducted for three days, and the replaced culture solution is the neural stem cell condition culture solution. By means of the method, the differentiation efficiency is improved, and the maturity of the cells and growth of neural synapses of nerve cells are also improved. The cell apoptosis in SH-SY5Y treated through RA can be inhibited.

A method of forming an Integrated Circuit (IC) chip, the IC chip and an on-chip synaptic crossbar memory array. Chip devices are formed on a surface of a semiconductor wafer. A connective layer is formed above the chip devices. A bottom electrode layer is formed on the connective layer. A neuromorphic synapse layer is formed above the bottom electrode layer with each synapse on a bottom electrode. Upper electrodes are formed above the synapses and orthogonal to bottom electrode lines. Each synapse being beneath an upper electrode where the upper electrode crosses a bottom electrode. Upper electrodes are refractory metal and the bottom electrodes are copper, or vice versa.

Methods for inducing non-embryonic lesioned central nervous system neurons to survive, integrate, extend axons over long distances, induce intra-lesion ingrowth of neurons into the lesion from host tissue and form synapses in vivo. Pluripotent neural stem cells are grafted into the lesioned CNS tissue within a tissue adhesive suspension, optionally in the presence of growth factors. No modification of the neuronal regenerative inhibitory environment of the CNS is necessary.

The present invention encompasses compositions and methods that activate P2Y receptors for the increased production of new synapses in the central nervous system. The formulations of the invention may be administered to a healthy subject or to a subject in need thereof to restore synapses.

A time series classifying memory includes an enumerated group of synapses. Each synapse of the group has a junction including pre-synaptic emitters communicating with post synaptic receptors. A single pathway is input to each synapse of the group, and when innervated, stimulates the junctions. Each successive synapse has successively more post synaptic receptors according to a fixed ratio. At each junction, quanta of neurotransmitter emitted from the emitters bind with available receptors. When all the receptors at a junction have been bound, the junction goes refractory. The synapse adjacent to the last junction to go refractory is marked. During a training mode the mark is a Long Term Potentiation (LTP) mark. During a live mode the mark is a Short Term Potentiation (STP) mark. The input is classified upon successful correlation of the LTP mark with the STP mark. A clock operable with synaptic matrix models this process.

An electronic neuronal circuit system to model the interaction between the postsynaptic terminal of a first synapse between two neurons and the postsynaptic terminal of a second synapse between two neurons includes comparators to model the presynaptic neurons of the synapses, plurality of three diodes connected to the comparators to model synapses, an AND gate and latch to model the formation of functional link between the postsynaptic terminals, and timer-controlled latches for controlling the life-span of the inter-postsynaptic functional link, durations of re-activation of inter-postsynaptic functional link and flow of activity through the output postsynaptic dendritic terminals.