Table 1

Summary of potential new structural and functional imaging markers for CAA

Imaging markerEvidence of potential as a biomarker in CAALimitations
MRI visible perivascular spaces in the centrum semiovale (CSO-PVS)
  • Severe or high-grade CSO-PVS commonly observed in CAA19–22

  • Pilot data show that, in those with CAA, CSO-PVS severity is associated with Aβ burden (as measured by PiB)23

  • Non-specific (age-related); present in a number of other conditions24

Cortical atrophy
  • Thinner cortices in those with sporadic CAA compared with healthy controls; occipital, temporal, posterior parietal and medial frontal areas affected14 (figure 1)

  • Difficult to differentiate between atrophy secondary to parenchymal Aβ and that due to vascular Aβ in sporadic CAA

Visual functional MRI
  • Patients with CAA have abnormal BOLD responses to a visual stimulus (alternating checkerboard), with reduced response amplitude and prolonged time both to peak and to baseline15 25

  • Those with CAA show a decline in BOLD amplitude that is detectable at 1 year; longitudinal difference in BOLD amplitudes was significantly lower in CAA compared with controls26

  • Potentially of interest as a surrogate marker of vascular health in clinical trials

  • Clinical implications of this remain unclear; due to technical factors at this stage, this is predominantly a research tool limited to academic medical centres

Network measures
  • Lower global efficiency of brain network in those with CAA; occipital, parietal and posterior temporal lobes most affected103

  • Reduced efficiency correlated with Aβ burden (as measured by PiB) and impaired executive function and processing speed103

  • Global efficiency shows a longitudinal decline with time (1.3 years) in those with CAA, and is associated with deteriorating executive function104

  • Difficult to differentiate between network effects of parenchymal Aβ versus those due to vascular Aβ in sporadic CAA

  • Mainly a research tool limited to academic medical centres

Amyloid PET imaging using [11C] PiB-PET and [18F] compounds
  • In those with CAA, regions with high PiB retention area associated with subsequent haemorrhage27

  • Although PiB-PET may not reliably distinguish between patients and age-matched controls,28 early phase (1–6 min) uptake can do this29

  • The occipital/posterior cingulate ratio of PiB uptake is different for those with CAA versus those with AD29

  • PiB-PET and [18F] florbetapir binding is able to distinguish between CAA-associated ICH and hypertension-associated ICH30

  • Amyloid PET unable to differentiate between vascular and parenchymal Aβ

  • Diagnostic accuracy for CAA seems limited

  • Few data on change over time in CAA

  • Aβ, amyloid-beta; AD, Alzheimer’s disease; BOLD, blood-oxygen level-dependent; CAA, cerebral amyloid angiopathy; ICH, intracerebral haemorrhage; PET, positron emission tomography; PiB, Pittsburgh B compound.