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The association between hypertensive arteriopathy and cerebral amyloid angiopathy in spontaneously hypertensive stroke-prone rats

The association between hypertensive arteriopathy and cerebral amyloid angiopathy in spontaneously hypertensive stroke-prone rats
The association between hypertensive arteriopathy and cerebral amyloid angiopathy in spontaneously hypertensive stroke-prone rats

We aimed to test the hypothesis that in spontaneously hypertensive stroke-prone rats (SHRSP), non-amyloid cerebral small vessel disease/hypertensive arteriopathy (HA) results in vessel wall injury that may promote cerebral amyloid angiopathy (CAA). Our study comprised 21 male SHRSP (age 17–44 weeks) and 10 age- and sex-matched Wistar control rats, that underwent two-photon (2PM) imaging of the arterioles in the parietal cortex using Methoxy-X04, Dextran and cerebral blood flow (CBF) measurements. Our data suggest that HA in SHRSP progresses in a temporal and age-dependent manner, starting from small vessel wall damage (stage 1A), proceeding to CBF reduction (stage 1B), non-occlusive (stage 2), and finally, occlusive thrombi (stage 3). Wistar animals also demonstrated small vessel wall damage, but were free of any of the later HA stages. Nearly half of all SHRSP additionally displayed vascular Methoxy-X04 positivity indicative of cortical CAA. Vascular β-amyloid deposits were found in small vessels characterized by thrombotic occlusions (stage 2 or 3). Post-mortem analysis of the rat brains confirmed the findings derived from intravital 2PM microscopy. Our data thus overall suggest that advanced HA may play a role in CAA development with the two small vessel disease entities might be related to the same pathological spectrum of the aging brain.

cerebral amyloid angiopathy, cerebral small vessel disease, hypertensive arteriopathy, intravital imaging, spontaneously hypertensive stroke-prone rat
1015-6305
Jandke, Solveig
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Garz, Cornelia
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Schwanke, Daniel
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Sendtner, Michael
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Heinze, Hans Jochen
e5b52444-3fcb-4abc-be1c-416bf91d7986
Carare, Roxana O.
0478c197-b0c1-4206-acae-54e88c8f21fa
Schreiber, Stefanie
0d270570-e83c-46e5-b241-04deeb2d1767
Jandke, Solveig
93edb572-ac6a-4696-9a56-e5b464bb40d5
Garz, Cornelia
beb2ed6d-1934-4742-8693-2f433c5b9b69
Schwanke, Daniel
067760cc-422f-4d7e-9dbb-47b451d66dac
Sendtner, Michael
00f80b6a-c6a3-4191-8f66-6343fce3811d
Heinze, Hans Jochen
e5b52444-3fcb-4abc-be1c-416bf91d7986
Carare, Roxana O.
0478c197-b0c1-4206-acae-54e88c8f21fa
Schreiber, Stefanie
0d270570-e83c-46e5-b241-04deeb2d1767

Jandke, Solveig, Garz, Cornelia, Schwanke, Daniel, Sendtner, Michael, Heinze, Hans Jochen, Carare, Roxana O. and Schreiber, Stefanie (2018) The association between hypertensive arteriopathy and cerebral amyloid angiopathy in spontaneously hypertensive stroke-prone rats. Brain Pathology. (doi:10.1111/bpa.12629).

Record type: Article

Abstract

We aimed to test the hypothesis that in spontaneously hypertensive stroke-prone rats (SHRSP), non-amyloid cerebral small vessel disease/hypertensive arteriopathy (HA) results in vessel wall injury that may promote cerebral amyloid angiopathy (CAA). Our study comprised 21 male SHRSP (age 17–44 weeks) and 10 age- and sex-matched Wistar control rats, that underwent two-photon (2PM) imaging of the arterioles in the parietal cortex using Methoxy-X04, Dextran and cerebral blood flow (CBF) measurements. Our data suggest that HA in SHRSP progresses in a temporal and age-dependent manner, starting from small vessel wall damage (stage 1A), proceeding to CBF reduction (stage 1B), non-occlusive (stage 2), and finally, occlusive thrombi (stage 3). Wistar animals also demonstrated small vessel wall damage, but were free of any of the later HA stages. Nearly half of all SHRSP additionally displayed vascular Methoxy-X04 positivity indicative of cortical CAA. Vascular β-amyloid deposits were found in small vessels characterized by thrombotic occlusions (stage 2 or 3). Post-mortem analysis of the rat brains confirmed the findings derived from intravital 2PM microscopy. Our data thus overall suggest that advanced HA may play a role in CAA development with the two small vessel disease entities might be related to the same pathological spectrum of the aging brain.

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Jandke_et_al-2018-Brain_Pathology - Version of Record
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More information

Accepted/In Press date: 2018
e-pub ahead of print date: 30 July 2018
Keywords: cerebral amyloid angiopathy, cerebral small vessel disease, hypertensive arteriopathy, intravital imaging, spontaneously hypertensive stroke-prone rat

Identifiers

Local EPrints ID: 425698
URI: http://eprints.soton.ac.uk/id/eprint/425698
ISSN: 1015-6305
PURE UUID: 168e225e-c346-498e-ac97-19517a68c4b3
ORCID for Roxana O. Carare: ORCID iD orcid.org/0000-0001-6458-3776

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Date deposited: 01 Nov 2018 17:30
Last modified: 26 Nov 2021 02:42

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Contributors

Author: Solveig Jandke
Author: Cornelia Garz
Author: Daniel Schwanke
Author: Michael Sendtner
Author: Hans Jochen Heinze
Author: Stefanie Schreiber

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