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Author Notes:

Correspondence to: Lary C. Walker, Department of Neurology, Emory University, 505M Whitehead Building, 615 Michael Street, Atlanta, GA 30322, USA, lary.walker@emory.edu

We thank Anil Mehta, David Lynn, and Yury Chernoff for helpful discussions, and Kaylor Kelly and Deborah Cooper for expert technical assistance.

The authors have no conflict of interest to report.

Subjects:

Research Funding:

This work was supported by National Institutes of Health (NIH) grants P50 AG025688, RR00165, and OD11132.

The NACC database is funded by NIA/NIH Grant U01 AG016976. NACC data are contributed by the NIA-funded ADCs: P30 AG019610 (PI Eric Reiman, MD), P30 AG013846 (PI Neil Kowall, MD), P50 AG008702 (PI Scott Small, MD), P50 AG025688 (PI Allan Levey, MD, PhD), P50 AG047266 (PI Todd Golde, MD, PhD), P30 AG010133 (PI Andrew Saykin, PsyD), P50 AG005146 (PI Marilyn Albert, PhD), P50 AG005134 (PI Bradley Hyman, MD, PhD), P50 AG016574 (PI Ronald Petersen, MD, PhD), P50 AG005138 (PI Mary Sano, PhD), P30 AG008051 (PI Thomas Wisniewski, MD), P30 AG013854 (PI M. Marsel Mesulam, MD), P30 AG008017 (PI Jeffrey Kaye, MD), P30 AG010161 (PI David Bennett, MD), P50 AG047366 (PI Victor Henderson, MD, MS), P30 AG010129 (PI Charles DeCarli, MD), P50 AG016573 (PI Frank LaFerla, PhD), P50 AG005131 (PI James Brewer, MD, PhD), P50 AG023501 (PI Bruce Miller, MD), P30 AG035982 (PI Russell Swerdlow, MD), P30 AG028383 (PI Linda Van Eldik, PhD), P30 AG053760 (PI Henry Paulson, MD, PhD), P30 AG010124 (PI John Trojanowski, MD, PhD), P50 AG005133 (PI Oscar Lopez, MD), P50 AG005142 (PI Helena Chui, MD), P30 AG012300 (PI Roger Rosenberg, MD), P30 AG049638 (PI Suzanne Craft, PhD), P50 AG005136 (PI Thomas Grabowski, MD), P50 AG033514 (PI Sanjay Asthana, MD, FRCP), P50 AG005681 (PI John Morris, MD), P50 AG047270 (PI Stephen Strittmatter, MD, PhD).

Keywords:

  • Science & Technology
  • Life Sciences & Biomedicine
  • Neurosciences
  • Neurosciences & Neurology
  • A beta
  • aging
  • amyloid
  • cerebrovascular amyloidosis
  • dementia
  • ethnicity
  • race
  • tauopathy
  • vascular disease
  • MILD COGNITIVE IMPAIRMENT
  • VASCULAR RISK-FACTORS
  • APOLIPOPROTEIN-E
  • NEUROPATHOLOGIC ASSESSMENT
  • ATHEROSCLEROSIS RISK
  • EMERGING CONCEPTS
  • BRAIN DONATION
  • ETHNIC-GROUPS
  • DEMENTIA
  • PATHOLOGY

Cerebral Amyloid Angiopathy: Similarity in African-Americans and Caucasians with Alzheimer's Disease

Tools:

Journal Title:

Journal of Alzheimer's Disease

Volume:

Volume 62, Number 4

Publisher:

, Pages 1815-1826

Type of Work:

Article | Post-print: After Peer Review

Abstract:

Cerebral amyloid angiopathy (CAA) of the Aβ type is variably present in the brains of patients with Alzheimer's disease (AD). CAA contributes to cognitive decline and increases the risk of lobar hemorrhage; because both AD-typical dementia and lobar hemorrhage are more common in African-Americans than in Caucasians, we postulated that African-Americans with AD might be particularly susceptible to CAA. To test this hypothesis, we analyzed CAA histopathologically in the large vessels and capillaries of autopsy-derived frontal, temporal, parietal, and occipital cortical samples from African-Americans (n = 18) and Caucasians (n = 19) with end-stage AD. In the combined cohort of 37 subjects, 22% of the subjects had severe CAA in large vessels, and 11% had severe CAA in capillaries. However, the prevalence and histopathologic characteristics of CAA were similar in the African-Americans and Caucasians. This conclusion was substantiated in an independent sample from the National Alzheimer's Coordinating Center database, in which the degree of CAA was comparable in 1,554 Caucasians and 68 African-Americans with end-stage AD. These findings support a growing consensus that the fundamental histopathologic features of AD are largely impartial to the race of the afflicted.

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©2018 IOS Press All rights reserved.

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