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Ann Clin Transl Neurol. 2014 Feb;1(2):124-9. doi: 10.1002/acn3.27. Epub 2014 Jan 9.

Hypertension drives parenchymal β-amyloid accumulation in the brain parenchyma.

Author information

1
Department of Neurology, Otto-von-Guericke University Magdeburg, Germany ; German Center for Neurodegenerative Diseases (DZNE) Magdeburg, Germany.
2
Faculty of Medicine, University of Southampton Southampton, United Kingdom.
3
Department of Neurology, Otto-von-Guericke University Magdeburg, Germany.
4
Institute for Aging and Health, Newcastle University Newcastle, United Kingdom.
5
Helen Wills Neuroscience Institute and Department of Psychology, University of California Berkeley, California.
6
German Center for Neurodegenerative Diseases (DZNE) Magdeburg, Germany.

Abstract

There is substantial controversy regarding the causative role of amyloid β (Aβ) deposition in Alzheimer's disease (AD). The cerebrovasculature plays an important role in the elimination of Aβ from the brain and hypertension is a well-known risk factor for AD. In spontaneously hypertensive stroke-prone rats (SHRSP), an animal model of chronic arterial hypertension, cerebral small vessel disease (CSVD) leads to age-dependent parenchymal Aβ accumulation similar to that observed in AD. These data approve the neuropathological link between CSVD and AD, confirm the challenge that parenchymal Aβ deposition is a specific marker for AD and disclose the meaning of SHRSP as valid experimental model to investigate the association between hypertension, CSVD, and Aβ plaques.

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