Research Foundation for Mental Hygiene, Inc.

Khalid Iqbal

Inge Grundke-Iqbal

Herbert Mossler

Herbert Mösler

Michael Flory

Sonia Chalbot

Inge Grundke-Ighal

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 Tyris 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.

Treatment of tauopathies with mGluR5 antagonists

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&#xd7;Tg-AD mice, a generally accepted mouse model of Alzheimer's disease and frontotemporal dementia in humans.

Treatment of tauopathies by passive immunization targeting the N-terminal projection domain of tau

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.

Neurogenic brain-derived neurotrophic factor peptides

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.

Treatment of autism spectrum disorders with ciliary neurotrophic factor peptide mimetic

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.

Neurotrophic peptides for the treatment of tauopathies

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.

Treatment of brain injury with a neurotrophic peptide

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.

Neurotrophic peptides

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.

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.

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.

Method for evaluating blood-neural barrier permeability

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).

A method for diagnosing distinct subgroups of Alzheimer's Disease, the method comprising the steps of obtaining a sample of cerebrospinal fluid and determining the level of ubiquitin, the level of A&#x3b2;, and the level of tau present in the sample. Based on the levels of each composition in the cerebrospinal fluid, the sample can be assigned to distinct subgroups.

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Staten Island, NY, United States of America

Khalid Iqbal