Abstract: The present disclosure relates to methods of inhibiting reactive astrocyte mediated neuronal and/or oligodendrocyte cell death in a subject. In one embodiment, the method involves administering an inhibitor of Elongation of Very Long Chain Fatty Acids Protein 1 (ELOVL1) to a subject having or at risk of having a condition mediated by reactive astrocytes, where the ELOVL1 inhibitor is administered in an amount effective to inhibit reactive astrocyte mediated neuronal and/or oligodendrocyte cell death in the subject. In another embodiment, the method involves administering an inhibitor of lipoapoptosis to a subject having or at risk of having a condition mediated by reactive astrocytes, where the inhibitor of lipoapoptosis is administered in an amount effective to inhibit reactive astrocyte mediate neuronal and/or oligodendrocyte cell death in the subject.

Abstract: Human pluripotent stem cells are differentiated in vitro into human cortical spheroids (hCS), which contain astrocytes, as well as cortical progenitors and neurons for use in analysis, screening programs, and the like.

Abstract: Provided are methods of modulating neuronal and/or oligodendrocyte survival. The subject methods relate to preventing neuronal and/or oligodendrocyte death or increasing neuron or oligodendrocyte death. Also provided are neuroprotective compositions and neurotoxic compositions. Methods of identifying neurotoxins, methods of identifying neurotoxin inhibitors and methods of identifying neurotoxin conditions in a subject 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 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 treating and preventing neurodegenerative diseases such as Alzheimer's disease.

Abstract: Compositions and methods are provided for the purification of astrocytes from biological samples or from in vitro cultures. An advantage of the methods of the invention is the ability to isolate astrocytes in a quiescent state, which allows analysis of the cells in a more natural state.

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: Compositions and methods are provided for the purification of astrocytes from biological samples or from in vitro cultures. An advantage of the methods of the invention is the ability to isolate astrocytes in a quiescent state, which allows analysis of the cells in a more natural state.

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: 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 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: 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: 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: 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: 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: 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: 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: 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: 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.