Abstract: The present invention describes methods and compositions for modulating synaptogenesis and axon and/or dendritic growth. The methods include the use of agents that modulate a thrombospondin and/or an ?2? subunit of a calcium channel.

Abstract: Methods are provided for enhancing myelination. Myelination is enhanced by administration of agents that are inhibitors of ?-secretase. Methods of screening for pharmaceutically active compounds that enhance myelination, and for genes involved in myelination are also provided.

Abstract: C1q is shown to be expressed in neurons, where it acts as a signal for synapse elimination. Methods are provided for protecting or treating an individual suffering from adverse effects of synapse loss. These findings have broad implications for a variety of clinical conditions, including treating and preventing neurodegenerative diseases such as Alzheimer's disease.

Abstract: C1q is shown to be expressed in neurons, where it acts as a signal for synapse elimination. Methods are provided for protecting or treating an individual suffering from adverse effects of synapse loss. These findings have broad implications for a variety of clinical conditions, including Alzheimer's disease.

Abstract: This invention relates to the 5-cis and 5-trans isomers of geranylgeranyl acetone, preferably such synthetic isomers, and pharmaceutical compositions containing such isomers. Other aspects of this invention relate to the use of geranylgeranyl acetone and its isomers in methods for inhibiting neural death, increasing neural activity, and increasing axon growth and cell viability. Geranylgeranyl acetone is a known anti-ulcer drug used commercially and in clinical situations. GGA has also been shown to exert cytoprotective effects on a variety of organs, such as the eye, brain, and heart.

Abstract: C1q is shown to be expressed in neurons, where it acts as a signal for synapse elimination. Methods are provided for protecting or treating an individual suffering from adverse effects of synapse loss. These findings have broad implications for a variety of clinical conditions, including Alzheimer's disease.

Abstract: Methods are provided for enhancing myelination. Myelination is enhanced by administration of agents that are inhibitors of ?-secretase. Methods of screening for pharmaceutically active compounds that enhance myelination, and for genes involved in myelination are also provided.

Abstract: The present invention provides compositions and methods for regulating neural cell proliferation or differentiation. The present invention also provides methods for selecting for bioactive agents effective in regulating proliferation or differentiation.

Abstract: Activation of the Wnt signaling pathway in cells is inhibited by contacting the cells with an Apcdd peptide. Wnt inhibition by this and other methods finds particular use in treating Wnt-mediated disease conditions such as conditions associated with aberrant angiogenesis in the CNS or aberrant cell proliferation.

Abstract: The present invention provides compositions and methods for regulating remyelination and promoting oligodendrocyte differentiation by modulating GM98 (also known as MRF) expression and activity. Compositions and methods for treating neuropathies and screening for bioactive agents are also provided herein.

Abstract: Methods are provided for enhancing myelination. Myelination is enhanced by administration of agents that are inhibitors of ?-secretase. Methods of screening for pharmaceutically active compounds that enhance myelination, and for genes involved in myelination are also provided.

Abstract: Soluble proteins, e.g. thrombospondins, can trigger synapse formation. Such proteins are synthesized in vitro and in vivo by astrocytes, which therefore have a role in synaptogenesis. These thrombospondins are only expressed in the normal brain exactly during the period of developmental synaptogenesis, being off in embryonic brain and adult brain but on at high levels in postnatal brain. Methods are provided for protecting or treating an individual suffering from adverse effects of deficits in synaptogenesis, or from undesirably active synaptogenesis. These findings have broad implications for a variety of clinical conditions, including traumatic brain injury, epilepsy, and other conditions where synapses fail to form or form inappropriately. Synaptogenesis is enhanced by contacting neurons with agents that are specific agonists or antagonists of thrombospondins. Conversely, synaptogenesis is inhibited by contacting neurons with inhibitors or antagonists of thrombospondins.

Abstract: The present invention describes methods and compositions for modulating synaptogenesis and axon and/or dendritic growth. The methods include the use of agents that modulate a thrombospondin and/or an ?2? subunit of a calcium channel.

Abstract: The present invention provides compositions and methods for regulating neural cell proliferation or differentiation. The present invention also provides methods for selecting for bioactive agents effective in regulating proliferation or differentiation.

Abstract: The present invention provides compositions and methods for regulating neural cell proliferation or differentiation. The present invention also provides methods for selecting for bioactive agents effective in regulating proliferation or differentiation.

Abstract: Soluble proteins, e.g. thrombospondins, can trigger synapse formation. Such proteins are synthesized in vitro and in vivo by astrocytes, which therefore have a role in synaptogenesis. These thrombospondins are only expressed in the normal brain exactly during the period of developmental synaptogenesis, being off in embryonic brain and adult brain but on at high levels in postnatal brain. Methods are provided for protecting or treating an individual suffering from adverse effects of deficits in synaptogenesis, or from undesirably active synaptogenesis. These findings have broad implications for a variety of clinical conditions, including traumatic brain injury, epilepsy, and other conditions where synapses fail to form or form inappropriately. Synaptogenesis is enhanced by contacting neurons with agents that are specific agonists or antagonists of thrombospondins. Conversely, synaptogenesis is inhibited by contacting neurons with inhibitors or antagonists of thrombospondins.

Abstract: The present invention provides compositions and methods for regulating neural cell proliferation or differentiation. The present invention also provides methods for selecting for bioactive agents effective in regulating proliferation or differentiation.

Abstract: Soluble proteins, e.g. thrombospondins, can trigger synapse formation. Such proteins are synthesized in vitro and in vivo by astrocytes, which therefore have a role in synaptogenesis. These thrombospondins are only expressed in the normal brain exactly during the period of developmental synaptogenesis, being off in embryonic brain and adult brain but on at high levels in postnatal brain. Methods are provided for protecting or treating an individual suffering from adverse effects of deficits in synaptogenesis, or from undesirably active synaptogenesis. These findings have broad implications for a variety of clinical conditions, including traumatic brain injury, epilepsy, and other conditions where synapses fail to form or form inappropriately. Synaptogenesis is enhanced by contacting neurons with agents that are specific agonists or antagonists of thrombospondins. Conversely, synaptogenesis is inhibited by contacting neurons with inhibitors or antagonists of thrombospondins.

Abstract: The present invention describes methods and compositions for modulating synaptogenesis and axon and/or dendritic growth. The methods include the use of agents that modulate a thrombospondin and/or an ?2? subunit of a calcium channel.

Abstract: Soluble proteins, e.g. Hevin, can trigger synapse formation; and other soluble proteins, e.g. SPARC antagonize this activity. Such proteins are synthesized in vitro and in vivo by astrocytes. Methods are provided for protecting or treating an individual suffering from adverse effects of deficits in synaptogenesis, or from undesirably active synaptogenesis.