Astrocytic transporters in Alzheimer's disease

Author:

Ugbode Chris1,Hu Yuhan2,Whalley Benjamin2,Peers Chris3,Rattray Marcus4,Dallas Mark L.2

Affiliation:

1. Department of Biology, University of York, Heslington, York YO10 5DD, U.K.

2. School of Pharmacy, University of Reading, Reading RG6 6UB, U.K.

3. School of Medicine, University of Leeds, Leeds LS2 9JT, U.K.

4. School of Pharmacy, University of Bradford, Bradford BD7 1DP, U.K.

Abstract

Astrocytes play a fundamental role in maintaining the health and function of the central nervous system. Increasing evidence indicates that astrocytes undergo both cellular and molecular changes at an early stage in neurological diseases, including Alzheimer's disease (AD). These changes may reflect a change from a neuroprotective to a neurotoxic phenotype. Given the lack of current disease-modifying therapies for AD, astrocytes have become an interesting and viable target for therapeutic intervention. The astrocyte transport system covers a diverse array of proteins involved in metabolic support, neurotransmission and synaptic architecture. Therefore, specific targeting of individual transporter families has the potential to suppress neurodegeneration, a characteristic hallmark of AD. A small number of the 400 transporter superfamilies are expressed in astrocytes, with evidence highlighting a fraction of these are implicated in AD. Here, we review the current evidence for six astrocytic transporter subfamilies involved in AD, as reported in both animal and human studies. This review confirms that astrocytes are indeed a viable target, highlights the complexities of studying astrocytes and provides future directives to exploit the potential of astrocytes in tackling AD.

Publisher

Portland Press Ltd.

Subject

Cell Biology,Molecular Biology,Biochemistry

Reference266 articles.

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