Affiliations: Menzies Research Institute, University of Tasmania, Hobart, Tasmania, Australia
Correspondence:
[*]
Correspondence to: Dr. Adele Vincent, Menzies Research Institute, Medical Science 1 Building, Private Bag 23, Hobart TAS 7000, Australia. Tel.: +61 3 6226 7195; Fax: +61 3 6226 7704; E-mail: Adele.Vincent@utas.edu.au. Professor David Small, Menzies Research Institute, Medical Science 1 Building, Private Bag 23, Hobart TAS 7000, Australia. Tel.: +61 3 6226 7348; Fax: +61 3 6226 7704; E-mail: D.H.Small@utas.edu.au.
Abstract: Alzheimer's disease (AD) is caused by the accumulation of amyloid-β (Aβ), which induces progressive decline in learning, memory, and other cognitive functions. Aβ 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 Aβ 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. Aβ can disrupt astrocytic calcium signaling and gliotransmitter release, processes that are vital for astrocyte-neuron 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.
