Abstract: 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.

Abstract: A method of treating tau pathologies, such as Alzheimer's disease, involving the administration of antibodies specific to the amino terminal region of human tau (amino acid residues 6-18 or 184-195) to provide passive immunization. The administration of such antibodies can reduce total tau levels, decrease tau hyperphosphorylation, and improve reference memory. Passive immunization with antibodies targeting the N-terminal projection domain of tau reduces both total and hyperphosphorylated tau was found effective in aged 3×Tg-AD mice, a generally accepted mouse model of Alzheimer's disease and frontotemporal dementia in humans.

Abstract: Five tetra peptides corresponding to different active regions of brain derived neurotrophic factor (BDNF) that are neurotrophic and can modulate BDNF signaling in a partial agonist/antagonist way. The peptides offer a therapeutic approach to neural pathologies where BDNF levels are dysregulated.

Abstract: 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.

Abstract: Five tetra peptides corresponding to different active regions of brain derived neurotrophic factor (BDNF) that are neurotrophic and can modulate BDNF signaling in a partial agonist/antagonist way. The peptides offer a therapeutic approach to neural pathologies where BDNF levels are dysregulated.

Abstract: Five tetra peptides corresponding to different active regions of brain derived neurotrophic factor (BDNF) that are neurotrophic and can modulate BDNF signaling in a partial agonist/antagonist way. The peptides offer a therapeutic approach to neural pathologies where BDNF levels are dysregulated.

Abstract: 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.

Abstract: Peptide 6 and in particular, Peptide 021, may be used to treat tauopathies, such as frontotemporal dementia with Parkinsonism linked to chromosome-17 (FTDP-17) tau, corticobasal degeneration, Pick disease, progressive supranuclear palsy, Guam Parkinsonism dementia complex, dementia pugilistica also known as traumatic encephalopathy or traumatic brain injury, ceroid neuronal lipofusinosis, Hallerworden Sptaz disease, Alzheimer's disease, and adults with Down syndrome.

Abstract: A method of treating tau pathologies, such as Alzheimer's disease, involving the administration of antibodies specific to the amino terminal region of human tau (amino acid residues 6-18 or 184-195) to provide passive immunization. The administration of such antibodies can reduce total tau levels, decrease tau hyperphosphorylation, and improve reference memory. Passive immunization with antibodies targeting the N-terminal projection domain of tau reduces both total and hyperphosphorylated tau was found effective in aged 3×Tg-AD mice, a generally accepted mouse model of Alzheimer's disease and frontotemporal dementia in humans.

Abstract: A neurotrophic peptide having the sequence VGDGGLFEKKL (SEQ ID NO: 1) may be used to help sustain local microenvironment after mild-to-moderate brain injury. Treatment with the peptide was shown to enhance differentiation of newly born progenitors in the dentate gyrus 30 days after injury and to promote neuronal maturation and survival that is not seen naturally after traumatic brain injuries.

Abstract: A neurotrophic peptide having the sequence VGDGGLFEKKL (SEQ ID NO: 1) may be used to help sustain local microenvironment after mild-to-moderate brain injury. Treatment with the peptide was shown to enhance differentiation of newly born progenitors in the dentate gyrus 30 days after injury and to promote neuronal maturation and survival that is not seen naturally after tramautic brain injuries.

Abstract: Peptide 6 and in particular, Peptide 021, may be used to treat tauopathies, such as frontotemporal dementia with Parkinsonism linked to chromosome-17 (FTDP-17) tau, corticobasal degeneration, Pick disease, progressive supranuclear palsy, Guam Parkinsonism dementia complex, dementia pugilistica also known as traumatic encephalopathy or traumatic brain injury, ceroid neuronal lipofusinosis, Hallerworden Sptaz disease, Alzheimer's disease, and adults with Down syndrome.

Abstract: 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.

Abstract: 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 Down syndrome.

Abstract: Five tetra peptides corresponding to different active regions of brain derived neurotrophic factor (BDNF) that are neurotrophic and can modulate BDNF signaling in a partial agonist/antagonist way. The peptides offer a therapeutic approach to neural pathologies where BDNF levels are dysregulated.

Abstract: The present invention relates to a neurotrophic peptide having an amino acid sequence of VGDGGLFEKKL (SEQ ID NO:1), EDQQVHFTPTEG (SEQ ID NO:2) or IPENEADGMPATV (SEQ ID NO:3), and comprising an adamantyl group at the C- and/or N-terminal end.

Abstract: A system and method for evaluating blood-neural barrier permeability. Phospholipid liposomes are labeled with a fluorescent phospholipase A2 substrate and exposed to cerebrospinal fluid. The change in fluorescence is monitored to determine PLA2 activity. The PLA2 activity is used to evaluate the permeability and function of the blood-neural barrier.

Abstract: The present invention relates to a neurotrophic peptide having an amino acid sequence selected from the group consisting of VGDGGLFEKKL (SEQ ID NO: 1), EDQQVHFTPTEG (SEQ ID NO: 2) and IPENEADGMPATV (SEQ ID NO: 3).

Abstract: Aminocyclohexane and aminoalkylcyclohexane compounds, which are systemically-active as NMDA receptor antagonists, are effective in inhibiting abnormal hyperphosphorylation of microtubule associated protein tau, method of treating disorders resulting from or associated with abnormal hyperphosphorylation of microtubule associated protein tau, and pharmaceutical compositions comprising the same.

Abstract: The present invention relates to a neurotrophic peptide having an amino acid sequence of VGDGGLFEKKL (SEQ ID NO:1), EDQQVHFTPTEG (SEQ ID NO:2) or IPENEADGMPATV (SEQ ID NO:3), and comprising an adamantyl group at the C- and/or N-terminal end.