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John M. Olichney, MD; Lawrence A. Hansen, MD; C. Richard Hofstetter, PhD; Michael Grundman, MD, MPH; Robert Katzman, MD; Leon J. Thal, MD

Arch Neurol. 1995;52(7):702-708.

Abstract
Objective
To determine if severe cerebral amyloid angiopathy (AA) in patients with Alzheimer's disease (AD) is associated with an increased prevalence of cerebral infarction diagnosed at autopsy. Amyloid angiopathy is increasingly recognized as a cause of ischemic infarcts, as well as cerebral hemorrhages. However, the relationship of AA to cerebral infarction in patients with AD is uncertain.

Design
Retrospective clinicopathological study of autopsy-confirmed cases of AD.

Patients
One hundred forty-five deceased patients with AD confirmed at autopsy.

Main Outcome Measures
Semiquantitative scores of AA severity were done in four brain regions: midfrontal, inferior parietal, superior temporal, and hippocampal. The finding of cerebral infarction at autopsy was modeled as a function of AA severity, hypertension, age at death, AD severity, and sex in X² and multiple logistic regression analyses.

Results
Severe AA was significantly associated with cerebral infarction at autopsy in patients with AD (odds ratio [OR], 3.5; 95% confidence interval [CI], 1.4 to 8.9). None of the other independent variables in the multiple logistic regression analysis were significant predictors. While hypertension was equally common in the severe and mild AA subgroups, the combination of both severe AA and hypertension interacted to increase the risk of infarction (OR, 14.2; 95% CI, 3.2 to 63.4) beyond that observed with hypertension (OR, 1.1; 95% CI, 0.4 to 3.2) or severe AA (OR, 1.3; 95% CI, 0.3 to 5.3) alone.

Conclusions
Severe AA is associated with an increased frequency of cerebral infarction in patients with AD. This appears to be largely due to an interaction between severe AA and hypertension that may produce multiplicative injuries on the vasculature. Further study with regard as to how AA may cause ischemia and its role in the neuropathologic and clinical progression of AD is needed.

Author Affiliations
From the Alzheimer's Disease Research Center (Drs Olichney, Hansen, Hofstetter, Grundman, Katzman, and Thai) and the Department of Neurosciences (Drs Olichney, Hansen, Grundman, Katzman, and Thai), University of California—San Diego, La Jolla, and the Neurology Service, Veterans Affairs Medical Center, San Diego (Drs Olichney and Thai).

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