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GLUT1 reductions exacerbate Alzheimer's disease vasculo-neuronal dysfunction and degeneration
Journal article   Peer reviewed

GLUT1 reductions exacerbate Alzheimer's disease vasculo-neuronal dysfunction and degeneration

Ethan A Winkler, Yoichiro Nishida, Abhay P Sagare, Sanket V Rege, Robert D Bell, David Perlmutter, Jesse D Sengillo, Sara Hillman, Pan Kong, Amy R Nelson, …
Nature neuroscience, Vol.18(4), pp.521-530
04/2015
DOI: 10.1038/nn.3966
PMCID: PMC4734893
PMID: 25730668
url
https://www.ncbi.nlm.nih.gov/pmc/articles/4734893View
Open Access

Abstract

The glucose transporter GLUT1 at the blood-brain barrier (BBB) mediates glucose transport into the brain. Alzheimer's disease is characterized by early reductions in glucose transport associated with diminished GLUT1 expression at the BBB. Whether GLUT1 reduction influences disease pathogenesis remains, however, elusive. Here we show that GLUT1 deficiency in mice overexpressing amyloid β-peptide (Aβ) precursor protein leads to early cerebral microvascular degeneration, blood flow reductions and dysregulation and BBB breakdown, and to accelerated amyloid β-peptide (Aβ) pathology, reduced Aβ clearance, diminished neuronal activity, behavioral deficits, and progressive neuronal loss and neurodegeneration that develop after initial cerebrovascular degenerative changes. We also show that GLUT1 deficiency in endothelium, but not in astrocytes, initiates the vascular phenotype as shown by BBB breakdown. Thus, reduced BBB GLUT1 expression worsens Alzheimer's disease cerebrovascular degeneration, neuropathology and cognitive function, suggesting that GLUT1 may represent a therapeutic target for Alzheimer's disease vasculo-neuronal dysfunction and degeneration.
Alzheimer Disease - physiopathology Cerebrovascular Circulation - physiology Mice, Inbred C57BL Blood-Brain Barrier - physiopathology Endothelium, Vascular - physiopathology Mice, Transgenic Alzheimer Disease - pathology Blood-Brain Barrier - metabolism Blood-Brain Barrier - pathology Animals Glucose Transporter Type 1 - deficiency Endothelium, Vascular - metabolism Alzheimer Disease - metabolism Amyloid beta-Peptides - metabolism Endothelium, Vascular - pathology Mice Disease Models, Animal

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