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Cerebral Amyloid Angiopathy in Alzheimer’s Disease and Related Disorders pp 265–279Cite as

Degeneration of Human Cerebrovascular Smooth Muscle Cells and Pericytes Caused by Amyloid β Protein

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Abstract

The deposition of amyloid β protein in the cerebral vasculature (also known as cerebral amyloid angiopathy, CAA, or congophilic angiopathy) is one of the neuropathological hallmarks of Alzheimer’s disease and several related disorders, such as hereditary cerebral hemorrhage with amyloidosis of the Dutch type. CAA can also occur independently of Alzheimer’s disease and is common in the brain of elederly individuals. When this condition develops in an advanced stage, it may be associated with cerebral hemorrhages and stroke. CAA-related brain hemorrhages often occur in association with brain microvascular alterations that include fibrinoid necrosis, microaneurysm formation and smooth muscle cell and pericyte death. In this review we summarize the relationship between amyloid β peptides and degeneration of smooth muscle cells and pericytes that have been studied in vitro. In particular, the effects of specific Aβ isoforms and the role of peptide fibril assembly in the induction of cellular degeneration and in increased cell-associated amyloid precursor protein has been extensively investigated. Evidence will be presented to demonstrate a differential response to different Aβ assembly states that mediate the toxic effect of the peptide on cerebrovascular cells on the one hand, and neurons on the other. These data suggest that there may be different recognition and/or pathogenic mechanisms for cells in the cerebrovascular compartment compared to neuronal cells.

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Author information

Authors and Affiliations

  1. Departments of Neurology, University Hospital Nijmegen, The Netherlands

    Marcel M. Verbeek

  2. Departments of Medicine and Pathology, Health Sciences Center, State University of New York, Stony Brook, NY, USA

    William E. Van Nostrand

  3. Departments of Pathology, University Hospital Nijmegen, The Netherlands

    Marcel M. Verbeek & Robert M. W. De Waal

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  1. Marcel M. Verbeek
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  2. William E. Van Nostrand
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  3. Robert M. W. De Waal
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Editors and Affiliations

  1. Departments of Neurology and Pathology, University Medical Center St. Radboud, Nijmegen, The Netherlands

    Marcel M. Verbeek

  2. Department of Pathology, University Medical Center St. Radboud, Nijmegen, The Netherlands

    Robert M. W. de Waal

  3. UCLA Medical Center, Los Angeles, CA, USA

    Harry V. Vinters

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Verbeek, M.M., Van Nostrand, W.E., De Waal, R.M.W. (2000). Degeneration of Human Cerebrovascular Smooth Muscle Cells and Pericytes Caused by Amyloid β Protein. In: Verbeek, M.M., de Waal, R.M.W., Vinters, H.V. (eds) Cerebral Amyloid Angiopathy in Alzheimer’s Disease and Related Disorders. Springer, Dordrecht. https://doi.org/10.1007/978-94-017-1007-7_16

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  • DOI: https://doi.org/10.1007/978-94-017-1007-7_16

  • Publisher Name: Springer, Dordrecht

  • Print ISBN: 978-90-481-5480-7

  • Online ISBN: 978-94-017-1007-7

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