Cardiovascular brain impulses in Alzheimer’s disease
Rajna, Zalán; Mattila, Heli; Huotari, Niko; Tuovinen, Timo; Krüger, Johanna; Holst, Sebastian C.; Korhonen, Vesa; Remes, Anne M.; Seppänen, Tapio; Hennig, Jürgen; Nedergaard, Maiken; Kiviniemi, Vesa (2021-03-31)
Zalán Rajna, Heli Mattila, Niko Huotari, Timo Tuovinen, Johanna Krüger, Sebastian C Holst, Vesa Korhonen, Anne M Remes, Tapio Seppänen, Jürgen Hennig, Maiken Nedergaard, Vesa Kiviniemi, Cardiovascular brain impulses in Alzheimer’s disease, Brain, Volume 144, Issue 7, July 2021, Pages 2214–2226, https://doi.org/10.1093/brain/awab144
© The Author(s) (2021). Published by Oxford University Press on behalf of the Guarantors of Brain. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.
https://creativecommons.org/licenses/by/4.0/
https://urn.fi/URN:NBN:fi-fe2021083044614
Tiivistelmä
Abstract
Accumulation of amyloid-β is a key neuropathological feature in brain of Alzheimer’s disease patients. Alterations in cerebral haemodynamics, such as arterial impulse propagation driving the (peri)vascular CSF flux, predict future Alzheimer’s disease progression. We now present a non-invasive method to quantify the three-dimensional propagation of cardiovascular impulses in human brain using ultrafast 10 Hz magnetic resonance encephalography. This technique revealed spatio-temporal abnormalities in impulse propagation in Alzheimer’s disease. The arrival latency and propagation speed both differed in patients with Alzheimer’s disease. Our mapping of arterial territories revealed Alzheimer’s disease-specific modifications, including reversed impulse propagation around the hippocampi and in parietal cortical areas. The findings imply that pervasive abnormality in (peri)vascular CSF impulse propagation compromises vascular impulse propagation and subsequently glymphatic brain clearance of amyloid-β in Alzheimer’s disease.
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