Cerebral amyloid angiopathy (CAA), which involves cerebrovascular deposition of β-amyloid (Aβ) proteins, is the major vascular aetiology underlying spontaneous lobar intracerebral haemorrhage (ICH) in elderly individuals.1 Aβ plaques in the parenchyma and neurofibrillary tangles comprised of hyperphosphorylated tau proteins are the histopathological hallmarks of Alzheimer’s disease. This evidence concerns the gene MAPT and early-onset autosomal dominant Alzheimer disease.