A retired medical editor aged 73 was referred to a neurologist by her PCP to evaluate a 3-year history of slowly progressive difficulty with recall and language expression, which she found very disturbing. Neurologic examination, neuropsychological testing, and amyloid PET imaging confirmed a diagnosis of mild cognitive impairment due to preclinical AD. She understood the probability of progression to AD over time and proactively asked about possible treatment options. She was willing to try one of the new, recently approved anti-amyloid monoclonal antibodies (anti-Aβ mAb), despite the fact that she was homozygous for ApoE ε4. Following a normal baseline brain MRI, she began treatment with lecanemab, which had just been approved by the FDA. Shortly after the 2nd infusion of lecanemab she developed severe, rapidly progressive symptoms including loss of central vision accompanied by severe headache, vertigo, and confusion. She was brought to the ED by ambulance, accompanied by her husband, where a brain MRI revealed severe ARIA-E and GRE/T2* images revealed multiple focal, round, very low-intensity microhemorrhages less than 10 mm in diameter compatible with severe amyloid-related imaging abnormalities (ARIA)-H. She was admitted to the neurology service for observation and management.