Abstract:
Disclosed herein are methods for treating juvenile onset neurological conditions, such as autism (ASD), intellectual disability, or epilepsy, with an inhibitor of N-methyl-D-aspartate receptor (NMDAR). The inhibitor may be NitroSynapsin or a derivative thereof.
Abstract:
The invention relates to a method of reducing neuronal injury or apoptosis including administering to a patient in need thereof an effective amount of a p38 mitogen-activated protein kinase (MAPK) inhibitor. Methods of treating an HIV-mediated dementia, glaucoma, or other neurodegenerative disorders are also disclosed.
Abstract:
El uso de un inhibidor de la proteína quinasa activada por mitógenos (MAPK) p38 en la fabricación de un medicamento para el tratamiento de pacientes que sufren glaucoma, neuropatía óptica, neuritis óptica, isquemia retinal, lesiones ópticas inducidas por láser, o vitreoretinopatía proliferativa inducida por cirugía o trauma; un paciente que sufre lesión neuronal o apoptosis que implique las células ganglionares de la retina; o un paciente que sufra un estado médico que provoque estrés nitrosativo u oxidativo a las células ganglionares de la retina por la activación excesiva de receptores aminoácidos excitatorios o la generación de radicales libres.
Abstract:
Disclosed are methods and compositions for identifying, producing, and using pathologically-activated targeting compounds. Pathologically- activated compounds are compound that only have an effect, or have a disproportionate effect, on a target molecule when a pathological condition exists.
Abstract:
This invention relates to Applicant’s discovery that Metabolic Syndrome, a cluster of disorders stemming from a resistance to insulin, contributes directly to dementia, particularly Alzheimer’s disease. Applicant’s invention includes a screening method to determine susceptibility and diagnosis of dementia based on the risk factors for Metabolic Syndrome. Applicant’s invention further includes methods for the prevention or treatment of dementia and other neurological conditions based on (1) minimizing insulin resistance, thereby preventing excess biosynthesis of insulin; (2) modulating the activity of IDE such that insulin competes less efficiently with β-amyloid protein for the IDE; and (3) blocking the consequences of NMDA receptor activation, such as by minimizing the generation of NO and other harmful free radicals.
Abstract:
The invention provides isolated N-methyl-D- aspartate type 3B (NR3B) polypeptides, functional fragments and peptides, encoding nucleic acid molecules and polynucleotides, and specific antibodies. Also provided are excitatory glycine receptors, containing either NR3B or NR3A polypeptides. Further provided are methods for detecting excitatory glycine receptor ligands, agonists and antagonists. The invention also provides related diagnostic and therapeutic methods.
Abstract:
Neurite outgrowth-promoting prostaglandins (NEPPs) and other electrophilic compounds bind to Keapl, a negative regulator of the transcription factor Nrf2, and prevent Keapl -mediated inactivation of Nrf2 and, thus, enhance Nrf2 translocation into the nucleus of neuronal cells. Therefore, neuroprotective compositions and related methods are provided that employ such neuroprotective compounds, and prodrugs of such compounds, to cause dissociation of Nrf2 from a Keapl /Nrf2 complex.
Abstract:
Disclosed are conjugates in which an aminoadamantane derivative, such as amantadine, memantine, or rimantadine is linked to a therapeutic agent. The conjugate can then be used to target the therapeutic agent to an injured neuron.
Abstract:
The present invention provides a method of providing acute neuroprotection by inducing the erythropoietin (EPO) signaling pathway in neuronal cells close to or subsequent to the time of excitatory insult; and inducing an insulin-like growth factor (IGF) signaling pathway in the neuronal cells close to or subsequent to the time of excitatory insult, thereby producing a synergistic acute neuropotective effect in the neuronal cells. The invention also provides a method of preventing or reducing the severity of a neurologic condition in a subject by administering to the subject EPO or an active fragment or analog thereof at a does of at most 200 U/kg; and administering to the subject an IGF or an active fragment or analog thereof, thereby providing of the neurologic condition. Such a method can be used to prevent or reduce the severity of, for example, Alzheimer's disease, Parkinson's disease, Huntington's disease, epilepsy, amyotrophic lateral sclerosis, multiple sclerosis, a movement disorder, HIV-associated dementia, HIV-associated neuropathy, neuropathicpain, migraine, glaucoma, drug addition, drug withdrawal, drug dependency, depression or anxiety.
Abstract:
The present invention provides a method of providing acute neuroprotection by inducing the erythropoietin (EPO) signaling pathway in neuronal cells close to or subsequent to the time of excitatory insult; and inducing an insulin-like growth factor (IGF) signaling pathway in the neuronal cells close to or subsequent to the time of excitatory insult, thereby producing a synergistic acute neuropotective effect in the neuronal cells. The invention also provides a method of preventing or reducing the severity of a neurologic condition in a subject by administering to the subject EPO or an active fragment or analog thereof at a does of at most 200 U/kg; and administering to the subject an IGF or an active fragment or analog thereof, thereby providing of the neurologic condition. Such a method can be used to prevent or reduce the severity of, for example, Alzheimer's disease, Parkinson's disease, Huntington's disease, epilepsy, amyotrophic lateral sclerosis, multiple sclerosis, a movement disorder, HIV-associated dementia, HIV-associated neuropathy, neuropathicpain, migraine, glaucoma, drug addition, drug withdrawal, drug dependency, depression or anxiety.