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Alzheimer’s disease (AD) is caused by the accumulation of amyloid  (A), which induces progressive decline in learning, memory, and other cognitive functions. A is a neurotoxic protein that disrupts calcium signaling in neurons and alters synaptic plasticity. These effects lead to loss of synapses, neural network dysfunction, and inactivation of neuronal signaling. However, the precise mechanism by which A causes neurodegeneration is still not clear, despite decades of intensive research. The role of astrocytes in early cognitive decline is a major component of disease pathology that has been poorly understood. Recent research suggests that astrocytes are not simply passive support cells for neurons, but are active participants in neural information processing in the brain. A can disrupt astrocytic calcium signaling and gliotransmitter release, processes that are vital for astrocyteneuron communication. Therefore, astrocyte dysfunction may contribute to the earliest neuronal deficits in AD. Here we discuss emerging concepts in glial biology and the implications of astrocyte dysfunction on neurodegeneration in AD.

Item Type:	Refereed Article
Keywords:	Glia, gliotransmitters, homeostatic plasticity, network dysfunction, neural networks, neurodegeneration, seizures, TNFá
Research Division:	Biomedical and Clinical Sciences
Research Group:	Neurosciences
Research Field:	Neurosciences not elsewhere classified
Objective Division:	Health
Objective Group:	Clinical health
Objective Field:	Clinical health not elsewhere classified
UTAS Author:	Vincent, AJ (Dr Adele Vincent)
UTAS Author:	Gasperini, R (Dr Rob Gasperini)
UTAS Author:	Foa, L (Professor Lisa Foa)
UTAS Author:	Small, DH (Professor David Small)
ID Code:	65209
Year Published:	2010
Web of Science® Times Cited:	57
Deposited By:	Menzies Institute for Medical Research
Deposited On:	2010-10-13
Last Modified:	2012-03-01
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