The papers summarized focus on Cerebral Amyloid Angiopathy (CAA), particularly the emerging clinical phenomenon of iatrogenic CAA (iCAA). iCAA is hypothesized to occur following the transmission of Amyloid-β (Aβ) seeds (prions) during medical procedures, such as neurosurgery involving cadaveric dura mater. Key points regarding CAA and iCAA include:• Pathogenesis and Latency: The transmission of Aβ results in symptomatic CAA decades later, with a typical latency between exposure and clinical onset ranging from 27 to 59 years.• Clinical Presentation: While initial reports focused on early-onset iCAA (typically under age 55) resulting from childhood procedures, later-onset cases (aged 65 and older) are now recognized, although differentiating them from sporadic CAA (sCAA) in this older age group remains challenging. Presenting symptoms often include spontaneous intracerebral hemorrhage (ICH), seizures, transient focal neurological episodes (TFNEs), or cognitive impairment.• Inflammatory Variant (CAA-ri): iCAA can evolve into CAA-related inflammation (CAA-ri), an acute or subacute encephalopathy characterized by features like headache, seizures, cognitive impairment, and specific MRI findings (e.g., asymmetric confluent white matter edema and leptomeningeal enhancement). CAA-ri in iCAA cases is often associated with a severe clinical course and may show a poor response to steroid treatment.• Diagnosis and Criteria: Diagnosis relies on clinical data and Magnetic Resonance Imaging (MRI) biomarkers, including lobar cerebral microbleeds (CMBs), cortical superficial siderosis (cSS), severe visible perivascular spaces in the centrum semiovale (CSO-PVS), and white matter hyperintensities (WMHs). The Boston Criteria version 2.0 for probable CAA incorporates these non-hemorrhagic MRI markers (like severe CSO-PVS and WMH-MS) to enhance diagnostic sensitivity without compromising specificity for sporadic CAA.