12 results about "Neuron loss" patented technology

The application discloses a fusion protein CHC targeting soluble IL-17RD, a preparation method and application thereof. The fusion protein CHC is formed by connecting and fusing two sIL-17RD neutralizing nanobodies CQ5 and CQ13 with human serum albumin (HSA) through a linker, and the structure is CQ5-Linker-CHC-Linker-CQ13, and the amino acid sequence is shown as SEQ ID NO. 1. The application further provides a gene sequence coding the fusion protein and an adeno-associated virus AAV-PHP.eB carrier containing the gene. The neutralizing nanobody fusion protein can specifically bind and neutralize the biological function of sIL-17RD, regulate the brain vascular endothelial cell homeostasis by directly inhibiting the inflammatory response of brain vascular endothelial cells induced by TNF-alpha and indirectly inhibiting the activation of microglial cells. The application can be used for treating or preventing neurodegenerative diseases such as Alzheimer's disease, and has the effects of protecting vascular injury, improving learning and memory and cognitive impairment, reducing beta-amyloid plaque deposition, reducing neuron loss and glial cell activation and the like.

The invention relates to the compound (2S,3S,4R,5R,6S,8R,9S,11R,15R)-3,5,15- triacetoxy-6(17)-epoxy-8-hydroxylathyrane-12E-en-14-one, also called (8R)-8-hydroxyepoxyboetirane A, as well as to a method for obtaining same and the use thereof to promote neuronal differentiation from neural precursors or neural stem cells in culture and in brain lesions. The invention also relates to the use of this compound to prepare a pharmaceutical composition that can be used to treat central nervous system lesions associated with neuron loss.

Disclosed is a use of artemether in preventing and treating Alzheimer's disease. Artemether is a safe and effective compound for treatment against malaria. Artemether activates an AMPK signaling pathway in the brain of a transgenic mouse model of Alzheimer's disease, improves learning and memory abilities in the mouse model, reduces neuron apoptosis in the brain, improves function of choline acetyltransferase, inhibits activity of glial cells, and reduces amyloid plaque deposition, neurofibrillary tangle, and neuron loss, thereby providing an experimental basis for clinical research on the treatment of Alzheimer's disease.

The application belongs to the technical field of biotechnology, and specifically discloses application of Olig2 in transdifferentiation of astrocytes into functional neurons, and provides overexpression of a neurogenesis-promoting transcription factor and knockdown of an inducible hindering factor, which are expected to be effective methods for improving transdifferentiation efficiency and generating more newborn neurons, and thus are widely applied to treatment of various nervous system diseases related to neuron loss, such as neurodegenerative diseases and traumatic diseases of the central nervous system.

Provided herein are methods for decreasing Ataxin-2 mRNA expression. Such methods are useful to ameliorate symptoms of Ataxin-2 associated diseases. Such Ataxin-2 associated diseases include amyotrophic lateral sclerosis (ALS). Such symptoms include loss of motor function, reduced CMAP amplitude, denervation, and loss of motor neurons.

New use of 1-amino-3,5-dimethyladamantane hydrochloride in treating or preventing cognitive impairment, reducing microglia in the cortex and hippocampus, reducing neuron loss in the cortex and hippocampus, and ameliorating the mitochondrial dysfunction state. The cognitive impairment includes cognitive impairment in systemic lupus erythematosus, Parkinson's disease, lateral sclerosis, stroke, multiple sclerosis, rheumatoid arthritis, inflammatory bowel disease, attention deficit hyperactivity disorder, sepsis-related encephalopathy, or mild cognitive disorder. The present application also provides a corresponding drug and a treatment or prevention method.

The invention relates to the technical field of medicines, in particular to application of coniferyl glycoside in treatment of neurodegenerative diseases. The medicine prepared from the product disclosed by the invention has the effects of improving cognitive function and inhibiting neurodegenerative change by reducing neuron loss and improving synaptic plasticity.

The invention discloses application of 2-methylthiazoline in preparation of a medicine for treating cerebral ischemia, and belongs to the technical field of biological medicine. The application of the 2-methylthiazoline in preparation of the medicine for treating cerebral ischemia is provided for the first time, by constructing a mouse middle cerebral artery embolism (MCAO) model and implementing a specific administration scheme, the remarkable effect of the 2-methylthiazoline is verified through multi-dimensional experiments, the 2-methylthiazoline can reduce the death rate of MCAO mice and adjust the postoperative body temperature, and the 2-methylthiazoline can be used for treating cerebral ischemia. Meanwhile, defect symptoms are improved from the nerve function level, pathological damage of brain tissue can be relieved, and neuron loss and cell apoptosis are reduced. The mechanism of action covers multiple dimensions of oxidative stress resistance, neuroinflammation inhibition and the like, the defects of narrow treatment time window, insufficient neuroprotective effect and the like of the existing cerebral ischemia treatment medicine can be specifically solved, and a novel scheme with clinical value and market potential is provided for cerebral ischemia treatment.

The invention provides a preparation method and application of a medicine for treating Parkinson's disease. The medicine for treating Parkinson's disease is prepared by taking ceramide as a target. According to the application, the ceramide is reduced through DES and GW, it is found that reduction of the ceramide can improve dyskinesia of Parkinson's disease model mice, neuronal loss is reduced, relevant indexes of mitochondria and autolysosome are recovered, and it is prompted that the targeted ceramide has a treatment effect on PLA2G6 related neurodegenerative diseases. Besides, DES and GW are used as ceramide inhibitors, and DES and GW respectively belong to aSMase and nSMase inhibitors, so that the application effect of DES and GW is remarkable and safe, and DES and GW have huge potential in treatment of PLA2G6-related Parkinson's disease.

The invention relates to the technical field of medicines, in particular to application of isofraxin in treatment of neurodegenerative diseases. The medicine prepared from the product disclosed by the invention has the effects of improving cognitive function and inhibiting neurodegenerative change by reducing neuron loss and improving synaptic plasticity.

The application discloses a kind of polypeptides for treating Parkinson's disease.In the application, it is first found that transient receptor potential M2 type (TRPM2) channel is more expressed in fragile DA neuron subgroup, and its expression amount is positively correlated with age in Parkinson's disease (PD) patient, and the mechanism of action is determined through rigorous experiment, i.e.TRPM2 channel is preferentially activated in ADE neuron through PARP-1 / PARG / ADPR axis, drives Mfn2 / Bcl-2 complex dependent mitochondrial superfusion, causes ADE neuron death.In addition, TRPM2 channel also drives MPTP treatment mouse SNc DA neuron susceptibility through Mfn2 / Bcl-2 mediation.Firstly, it is found that blocking PARP-1 / PARG / ADPR and Mfn2 / Bcl-2 mediated DA neuron death pathway can prevent the death of induced pluripotent stem cell (iPSC) derived DA neuron specific to spontaneous Parkinson's disease (SPD) patient.As susceptible SNc DA neuron loss is the main symptom of PD, therefore, PARP-1 / PARG / ADPR and Mfn2 / Bcl-2 pathway can become a new therapeutic target for PD.

The invention relates to application of polyphyllin II in preparation of a medicine for relieving learning and memory impairment induced by diethyl hexyl phthalate (DEHP). Aiming at neurotoxicity and cognitive defects caused by DEHP exposure, the invention reveals that the polyphyllin II plays roles through dual mechanisms: inhibiting release of inflammatory factors such as TNF-alpha, IL-6 and the like, down-regulating expression of TNFAIP1, activating a CREB signal channel and recovering protein levels of BDNF and Bcl-2; miR-93 expression is up-regulated, TNFAIP1 is inhibited in a targeted manner, and DEHP-induced synaptic plasticity injury is blocked. According to the technical scheme, polyphyllin II and DEHP are combined for use, and behavioristics and histology verify that the learning and memory ability of mice is remarkably improved (the incubation period is shortened, and the target quadrant residence time is recovered by 40% or above), neuron loss is reversed, and synaptic protein down-regulation is performed (the synaptic protein is recovered to a healthy group by 85% or above, plt, 0.01).