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Aβ protein is the main component of the amyloid of Alzheimer disease (AD) that builds up extracellularly in the neuropil as senile plaques (SP) and in the vessel walls as cerebral amyloid angiopathy (CAA) [14]. In some cases, CAA dominates pathologically over SP and this corresponds to a clinical presentation with multiple cerebral hemorrhages rather than degenerative dementia. The former can either present as a sporadic disease or as an hereditary condition (cerebral hemorrhage with amyloidosis, HCHWA) associated with specific APP mutations [3, 13]. Although the experimental seeding of Aβ is a well-known phenomenon [11], examples of Aβ transmission in humans have not been reported until recently. Amyloid Aβ transmission by a prion-like mechanism has been postulated at first on the basis of the neuropathological findings in patients with iatrogenic Creutzfeldt-Jakob disease [4, 12] and later in young adult individuals with early onset CAA who had a history of neurosurgery or other invasive medical procedures [2, 7–9]. In these papers, young adults (aged 30 to 57) have been reported in whom pathologically proven CAA has been linked with intrusive medical procedures performed some decades before consisting in neurosurgery with or without dura mater grafting and embolization of external carotid artery by dural extracts.

acta neuropathologica communications

Iatrogenic early onset cerebral amyloid angiopathy 30 years after cerebral trauma with neurosurgery: vascular amyloid deposits are made up of both Aβ40 and Aβ42