摘要:
The present invention provides a compound having the structure:
or a pharmaceutically acceptable salt or ester thereof, and a method of treating a subject afflicted with pain, a depressive disorder, a mood disorder or an anxiety disorder by administering the compound to the subject.
摘要:
A method of treating autism spectrum disorders using a therapeutic amount of a synthetic amino acid sequence corresponding to a portion of human ciliary neurotrophic factor (CNTF). In particular, the synthetic amino acid sequence is VGDGGLFEKKL (SEQ ID NO: 1), referred to as Peptide 6. Peptide 6 was tested and shown to exert a neuroprotective effect by modulating CNTF/JAK/STAT pathway and LIF signaling and enhancing brain derived neurotrophic factor (BDNF) expression.
摘要翻译:使用治疗量的对应于人睫状神经营养因子(CNTF)的一部分的合成氨基酸序列治疗自闭症谱系障碍的方法。 特别地,合成氨基酸序列是VGDGGLFEKKL(SEQ ID NO:1),被称为肽6.肽6被测试并显示出通过调节CNTF / JAK / STAT途径和LIF信号传导并增强脑源性的神经保护作用 神经营养因子(BDNF)表达。
摘要:
Intranasal administration of insulin for a predetermined period prior to anesthesia significantly prevented anesthesia-induced tau hyperphosphorylation and cognitive impairment and enhanced brain insulin signaling in mice. Intranasal insulin thus provides a treatment for prevention of anesthesia-induced tau pathology and increased risk for tauopathies in surgical patients and may be administered to a subject prior to anesthesia, such as by administering several doses of intranasal insulin for several consecutive days prior to any anesthesia.
摘要:
The present invention relates to a neurotrophic peptide having an amino acid sequence of VGDGGLFEKKL (SEQ ID NO: 1) and alternatively comprising an adamantyl group at the C-and/or N-terminal end. The neurotrophic peptide can rescue cognition, correct impairments in neural cell proliferation and synaptic plasticity, and thus address the cognitive defects associated with Alzheimer's disease.
摘要翻译:本发明涉及具有VGDGGLFEKKL(SEQ ID NO:1)氨基酸序列的神经营养肽,或者在C-和/或N-末端含有金刚烷基。 神经营养肽可以促进神经细胞增殖和突触可塑性的认知,正确的损伤,从而解决与阿尔茨海默病有关的认知缺陷。
摘要:
The treatment of age-related macular degeneration with the chronic administration of the neurotrophic peptidergic compound P021. Chronic treatment of animal models for age-related macular degeneration prevented the pathological changes associated with age-related macular degeneration, including photoreceptor degeneration, lipofuscin granules, vacuoles and atrophy in retinal pigment epithelium (RPE), Bruch's membrane (BM) thickening, rosette-like structure formation, microgliosis and astrogliosis.
摘要:
An assay for a GCH1 allele and associated genotype for the screening, prediction, diagnosis, prognosis, treatment and treatment response of psychiatric, neuropsychiatric, and neurological disorders, such as schizophrenia, schizoaffective disorder and bipolar disorder, and for defining treatments of such disorders. The presence of a variant in the GCH1 gene, alone or in conjunction with a measurement of low or altered biopterin, or altered BH4 system measures, is used to screen or diagnose subjects at risk for developing a psychiatric, neuropsychiatric, or neurological disorder. The genetic assay, with or without a biopterin or BH4 system assay, may also be used to determine treatment regimens. For subjects with an impaired BH4 system, treatments to increase or normalize biopterin, BH4, or the BH4 system can also be used, such as BH4 supplementation, lithium treatment, phenylalanine treatment, or other treatments and therapies.
摘要:
The treatment of abnormal hyperphosphorylation of tau in brains of patients with metabotropic glutamate receptor 5 (mGluR5) antagonists. The treatment uses the signaling pathway in which the inhibition of protein phosphatase 2A (PP2A) through phosphorylation of its catalytic subunit PP2Ac at Tyr307 is induced by the activation of metabotropic glutamate receptor 5 (mGluR5) and leads to hyperphosphorylation of tau. The mGluR5-PP2A axis has a central role in neurofibrillary degeneration and thus is be a therapeutic target for the treatment of tauopathies.
摘要:
Cerebral ischemia-reperfusion injury may be treated by compounds that increase brain O-GlcNAcylation, such as a therapeutic amount of a compound that increases the hexosamine biosynthesis pathway flux that bypasses glutamine/fructose-6-phosphate amidotransferase 2 or a therapeutic amount of a compound that inhibits OGA. The initial and transient elevation of brain O-GlcNAcylation is neuroprotective and helps ameliorate cerebral ischemia-reperfusion injury when administered within three hours of the ischemia-reperfusion-induced brain injury and continues for at least two days.