Before the bolus: why anti-amyloid therapy must become part of every stroke code.

Anti-amyloid monoclonal antibodies provide disease-modifying treatment options for selected patients with early symptomatic Alzheimer disease, but introduce new challenges for acute stroke care. Amyloid-related imaging abnormalities (ARIA) are often asymptomatic; however, symptomatic ARIA may cause aphasia, focal weakness, visual disturbance, confusion, headache, or seizures, and can resemble acute ischemic stroke. Initial noncontrast computed tomography may be nondiagnostic in both conditions, and failure to identify anti-amyloid exposure can complicate time-sensitive reperfusion decisions. Current regulatory guidance advises caution when considering thrombolytic therapy because serious and fatal intracerebral hemorrhage has been reported, although the absolute risk and a safe interval following anti-amyloid administration remain uncertain. Conversely, attributing every acute neurological deficit to ARIA could delay effective reperfusion for a true ischemic stroke. This editorial examines the clinical and imaging features relevant to this diagnostic overlap and proposes a systems-based response involving reliable medication identification, rapid vascular imaging, targeted magnetic resonance imaging, specialist collaboration, and separate consideration of intravenous thrombolysis and mechanical thrombectomy. Anti-amyloid exposure should be recognized as time-critical information during stroke evaluation. The objective is not automatic exclusion from reperfusion, but an individualized approach that minimizes avoidable hemorrhagic harm while preserving appropriate treatment for confirmed cerebral ischemia.