ESOC 2025 | Inflammatory CAA: pathophysiology and differentiating from similar diseases
Michele Romoli, MD, PhD, Bufalini Hospital, Cesena, Italy, comments on inflammatory cerebral amyloid angiopathy (CAA) as a new entity in the neurological landscape, characterized by inflammatory changes within the context of CAA. Dr Romoli highlights the importance of perivasculitis, a specific histopathological feature, in differentiating inflammatory CAA from Aβ-related angiitis, and notes that immunosuppression is the primary strategy for management. This interview took place at the 11th European Stroke Organisation Conference (ESOC) in Helsinki, Finland.
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Transcript
Yes, in a special session on the first day of the Congress, we will go through the inflammatory CAA, so the inflammatory phenotype of cerebral amyloid angiopathy. This is a, I would say, a rather new entity as is cerebral amyloid angiopathy, a new entity in the neurological panorama. So first of all, these are inflammatory changes in the context of cerebral amyloid angiopathy. These changes are defined from a neuro-radiological point of view and from a clinical point of view, but they also have specific histopathological features...
Yes, in a special session on the first day of the Congress, we will go through the inflammatory CAA, so the inflammatory phenotype of cerebral amyloid angiopathy. This is a, I would say, a rather new entity as is cerebral amyloid angiopathy, a new entity in the neurological panorama. So first of all, these are inflammatory changes in the context of cerebral amyloid angiopathy. These changes are defined from a neuro-radiological point of view and from a clinical point of view, but they also have specific histopathological features. And this means that this can be in some way different and differentiated from the standard cerebral amyloid angiopathy phenotype and from what is called the Aβ-related angiopathy and the vasculitis of the central nervous system or the primary angiitis of the central nervous system. This is mainly related to the deposit of Aβ, so the beta-amyloid, the same protein that is responsible also for part of the Alzheimer’s disease spectrum, which needs to be present and needs to create an inflammatory phenotype, which means that there is some perivasculitis. So no clear vasculitis, no overall vasculitis, no full-wall vasculitis, but just perivasculitis. And this is critical to differentiate inflammatory CAA from Aβ-related angiitis, because this is a full angiitis with a transmural approach. So the treatment and management of this condition will be discussed, but the main strategy we have at the moment is, in general, immunosuppression. We will go through potential recommendations for the management of these diseases and we will discuss with a panel of experts what to do when we have these kind of cases to manage.
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