The role of cerebrovascular disease when there is concomitant Alzheimer disease

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Abstract

Cerebrovascular Pathologies (CVP) are the most common co-existent pathologies observed in conjunction with Alzheimer disease. CVP rarely exists in isolation in later life, and CVP most likely plays a supporting role, rather than a sole leading role, in the pathogenesis of dementia. Our goal is to illustrate CVP's role using neuroimaging biomarkers. First, we discuss the frequency of CVP and present data from population-based Mayo Clinic Study of Aging. Here, we used a novel metric for identifying individuals with cerebrovascular imaging abnormalities (that we designate as "V. +") and present the frequency of V. -/V. + in the context of absence and presence of β-amyloid elevation (designated A. -/A. +). Next, we discuss the contribution of CVP to neurodegeneration and use hippocampal volume loss over time in a subset of participants categorized as A. - V. -, A. - V. +, A + V. -, A + V + Lastly, we discuss the contribution of CVP to cognitive impairment and conclude with the considerations for design of future studies.

Original languageEnglish (US)
JournalBiochimica et Biophysica Acta - Molecular Basis of Disease
DOIs
StateAccepted/In press - Jul 3 2015

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Cerebrovascular Disorders
Alzheimer Disease
Pathology
Amyloid
Neuroimaging
Dementia
Biomarkers
Population

ASJC Scopus subject areas

  • Molecular Biology
  • Molecular Medicine

Cite this

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abstract = "Cerebrovascular Pathologies (CVP) are the most common co-existent pathologies observed in conjunction with Alzheimer disease. CVP rarely exists in isolation in later life, and CVP most likely plays a supporting role, rather than a sole leading role, in the pathogenesis of dementia. Our goal is to illustrate CVP's role using neuroimaging biomarkers. First, we discuss the frequency of CVP and present data from population-based Mayo Clinic Study of Aging. Here, we used a novel metric for identifying individuals with cerebrovascular imaging abnormalities (that we designate as {"}V. +{"}) and present the frequency of V. -/V. + in the context of absence and presence of β-amyloid elevation (designated A. -/A. +). Next, we discuss the contribution of CVP to neurodegeneration and use hippocampal volume loss over time in a subset of participants categorized as A. - V. -, A. - V. +, A + V. -, A + V + Lastly, we discuss the contribution of CVP to cognitive impairment and conclude with the considerations for design of future studies.",
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