Abstract
The neurovascular unit (NVU) plays an important role in maintaining the function of the central nervous system (CNS). Emerging evidence has indicated that the NVU changes function and molecules at the early stage of Alzheimer’s disease (AD), which initiates multiple pathways of neurodegeneration. Cell types in the NVU have become attractive targets in the interventional treatment of AD. The NVU transportation system contains a variety of proteins involved in compound transport and neurotransmission. Brain transporters can be classified as members of the solute carrier (SLC) and ATP-binding cassette (ABC) families in the NVU. Moreover, the transporters can regulate both endogenous toxins, including amyloid-beta (Aβ) and xenobiotic homeostasis, in the brains of AD patients. Genome-wide association studies (GWAS) have identified some transporter gene variants as susceptibility loci for late-onset AD. Therefore, the present study summarizes changes in blood-brain barrier (BBB) permeability in AD, identifies the location of SLC and ABC transporters in the brain and focuses on major SLC and ABC transporters that contribute to AD pathology.
Highlights
Central nervous system (CNS) barriers are vital to the brain microenvironment for the regulation of neuronal functions, including nutrient transport and protection of the brain from toxins [1]
This review summarizes changes in bloodbrain barrier (BBB) permeability in Alzheimer’s disease (AD), identifies the location of solute carrier (SLC) and ATP-binding cassette (ABC) transporters in the brain and focuses on major SLC and ABC transporters that contribute to AD pathology
Claudin-5 and ZO-2 display a continuous distribution along the plasma membrane in cell-cell contacts, but brain endothelial cells treated with Aβ1–42 for 3 days cause tight junctions (TJs) protein relocation to the cytoplasm, decreased occludin expression and altered BBB integrity, contributing to the pathogenesis of AD [29]
Summary
Central nervous system (CNS) barriers are vital to the brain microenvironment for the regulation of neuronal functions, including nutrient transport and protection of the brain from toxins [1]. Brain transporters in the BBB can be classified as uptake transporters (including the solute carrier (SLC) superfamily) and efflux transporters (including the ATPbinding cassette (ABC) superfamily). These transporters are considered to play key roles in the treatment and pathogenesis of CNS disorders such as AD (Fig. 1) [5, 6]. Loss of BBB integrity and transporter dysfunction affect the entry or efflux of compounds, disrupting CNS homeostasis and thereby exacerbating CNS diseases, including AD and stroke. AD, a typical neurodegenerative disorder, is characterized by the presence of amyloid plaques and neurofibrillary tangles It is associated with microvascular dysfunction and/or degeneration in the brain [11]. This review summarizes changes in BBB permeability in AD, identifies the location of SLC and ABC transporters in the brain and focuses on major SLC and ABC transporters that contribute to AD pathology
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