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Neurology 2003;60:1020-1022
© 2003 American Academy of Neurology
Brief Communications

Hemorrhagic stroke associated with the Iowa amyloid precursor protein mutation

S. M. Greenberg, MD PhD, Y. Shin, MA, T. J. Grabowski, MD, G. E. Cooper, MD PhD, G. W. Rebeck, PhD, S. Iglesias, MD, F. Chapon, MD, E. Tournier–Lasserve, MD and J.-C. Baron, MD

From the Department of Neurology (Drs. Greenberg and Rebeck, Y. Shin), Massachusetts General Hospital and Harvard Medical School, Boston, MA; Department of Neurology and Radiology (Dr. Grabowski), College of Medicine, University of Iowa, Iowa City; Sanders–Brown Center on Aging (Dr. Cooper), University of Kentucky, Lexington; INSERM U320 (Drs. Chapon and Baron), University of Caen, France; INSERM EMI 99-21 (Dr. Tournier–Lasserve), Faculté de Medecine Lariboisiere and Hopital AP-HP Lariboisiere, Paris, France; and Department of Neurology (Dr. Baron), University of Cambridge, England.

Address correspondence and reprint requests to Dr. Steven M. Greenberg, Massachusetts General Hospital, Wang ACC 836, Boston, MA 02114; e-mail: greenberg{at}helix.mgh.harvard.edu

The authors searched for mutations in the ß-amyloid precursor protein in a Spanish family with a hereditary syndrome of hemorrhagic stroke, dementia, leukoencephalopathy, and occipital calcifications. DNA from two affected members demonstrated the Iowa amyloid precursor protein mutation previously identified as a cause of severe amyloid angiopathy without hemorrhagic stroke. These data point to other genetic or environmental factors that may determine the occurrence of symptomatic hemorrhage in amyloid angiopathy.




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