Welcome to the Allen lab

The goal of our work is to identify how non-neuronal glial cells, specifically astrocytes, regulate the formation, function and stability of neuronal synapses. Synapses are essential points of information transfer within neuronal circuits, and the correct formation and maturation of synapses is necessary for the brain to function throughout life. This is evident by the numerous neurological disorders where synaptic dysfunction is a key component, including autism, schizophrenia, bipolar disorder and Alzheimer’s disease.

Astrocytes constitute ~20% of cells in the brain and closely interact with neurons and synapses via thousands of fine processes, putting them in a position to sculpt the development of synapses and regulate ongoing synaptic transmission. As the brain progresses from early development to adulthood to aging, the properties of neurons and synapses change: from high levels of synaptogenesis and remodeling in development, to stable mature synapses in the adult brain, to synapse loss and a decline in synaptic function in aging. We aim to identify if these stage-specific properties of synapses are all intrinsic to neurons, or if the astrocytes the neurons interact with also display stage-specific properties that regulate synaptogenesis, synaptic stability and synapse loss.

Much of our research has focused on identifying how astrocytes regulate synapse formation and plasticity in the developing and adult brain, where we have made significant progress in identifying proteins secreted by astrocytes that induce de novo synaptogenesis between neurons during development, and induce synapse maturation and inhibit plasticity in the adult. Recently we have begun to ask if astrocytes contribute to synaptic dysfunction in aging, and identified that aging astrocytes alter their gene expression towards a program that will promote synapse loss. We now aim to determine the molecular mechanisms that astrocytes use to inhibit plasticity in the adult brain; the contribution of astrocytes to synapse loss and early stages of pathology in neurodegeneration; and whether astrocyte synaptogenic cues can be used to repair synapses in disorders where they are lost.