Amyloid β oligomers constrict human capillaries in Alzheimer’s disease via signaling to pericytes
Ross Nortley(University College London), Nils Korte(University College London), Pablo Izquierdo(University College London), Chanawee Hirunpattarasilp(University College London), Anusha Mishra(Oregon Health & Science University), Zane Jaunmuktane(National Hospital for Neurology and Neurosurgery), Vasiliki Kyrargyri(University College London), Thomas Pfeiffer(University College London), Lila Khennouf(University College London), Christian Madry(University College London), Hui Gong(University College London), Angela Richard-Loendt(National Hospital for Neurology and Neurosurgery), Wenhui Huang(Saarland University), Takashi Saito(RIKEN Center for Brain Science), Takaomi C. Saido(RIKEN Center for Brain Science), Sebastian Brandner(National Hospital for Neurology and Neurosurgery), Huma Sethi(National Hospital for Neurology and Neurosurgery), David Attwell(University College London)
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Abstract
Pericytes put the squeeze on cognition Like a computer, the brain needs a reliable source of power, which is provided as oxygen and glucose in the blood. However, in many neurological disorders this energy supply is disrupted. Brain blood flow is controlled by adjustment of the diameters of the vessels supplying the blood. Nortley et al. found that, both in humans developing Alzheimer's disease (AD) and in a mouse model of AD, brain capillaries become squeezed by pericytes (see the Perspective by Liesz). By defining the underlying mechanism, they suggest potential targets for therapy in early AD. Science , this issue p. eaav9518 ; see also p. 223
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