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Treatment of Alzheimer disease (AD) by infusion of antibodies against the β-amyloid peptide (Aβ) is currently in clinical trials. The rationale behind this passive immunotherapeutic approach is to clear or neutralize the amyloid peptide's toxic forms. Although determining efficacy at slowing or preventing AD progression is the primary focus of these trials, issues of the safety of anti-AD immunotherapy have also arisen. Approximately 10% of clinical trial subjects receiving the humanized anti-Aβ antibody bapineuzumab1 developed a condition termed vasogenic edema (VE), consisting of reversible T2-hyperintense signal on MRI in the white matter, leptomeninges, and sulci, sometimes associated with clinical symptoms such as headache, changes in mental status, vomiting, and gait disturbance. VE occurred more commonly in subjects receiving higher doses of antibody and in carriers of the APOE ϵ4 allele.
Although the pathogenesis of antibody-related VE remains undefined (with no neuropathologic findings yet reported), an intriguing possibility is that it results from an immune response directed toward cerebrovascular Aβ deposits (cerebral amyloid angiopathy [CAA]). There is evidence for this in the notable similarities between antibody-related VE and the syndrome of …
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