• Alzheimer’s disease
• amyloid angiopathy

In patients with Alzheimer’s disease (AD), focal and diffuse ischaemic abnormalities of the cerebral white matter can be demonstrated neuropathologically^1–3 and neuroradiologically.^4–8 The focal lesions have been shown to contribute to motor and neuropsychiatric manifestations of AD,^9–12 and the more widespread or diffuse abnormalities to impaired cognition.¹³¹⁴ In some series, ischaemic cerebral lesions in AD have been more frequent in patients homozygous or heterozygous for the epsilon 4 (e4) allele of the apolipoprotein E gene (APOE),^15–17 but other studies have found no such association,^18–21 Studies of the relation between white matter disease in patients with AD or probable AD, and the systemic manifestations of arteriosclerotic vascular disease, have yielded inconsistent findings.^11121–24

Several observations implicate cerebral amyloid angiopathy (CAA) as the probable cause of much of the white matter damage in AD. The vascular deposition of amyloid β protein (Aβ) is much more frequent and tends to be much more severe in patients with AD than in age-matched controls.^25–29 Furthermore, CAA is a well documented risk factor for cerebral infarction^1630–32 and for focal and diffuse white matter ischaemic lesions.^33–36 The mechanisms whereby CAA may cause ischaemic damage to the white matter probably include a combination of luminal stenosis, endothelial damage, basement membrane thickening, thrombosis, loss of autoregulation, and vasospasm.^37–40 Because evidence of the involvement of CAA in AD is largely based on post-mortem studies, which are by their nature skewed towards end stage disease, it could be argued that any contribution of CAA may be confined to the terminal stages of …