Neurodegenerative diseases are typically characterized by toxic deposits of proteins from brain metabolism. As such, amyloid-beta plaques and tau neurofibrillary tangles are hallmark lesions of Alzheimer disease (AD).1 Several amyloid-beta isoforms and tau protein seem to be excreted from brain along paravascular routes in free communication with the subarachnoid compartment and CSF. Recent studies have demonstrated that brain molecular clearance is highly dependent on CSF clearance to meningeal lymphatic vessels.2 MRI contrast agents do not readily cross the intact BBB in either direction; therefore, when a contrast agent is administered in CSF (intrathecally), it can be assumed to be confined outside the BBB. The MRI contrast agent may therefore serve as a surrogate marker and resemble extravascular distribution and clearance of other hydrophilic molecules, including some amyloid-beta isoforms and tau.
We obtained permission from the National Medicine Agency of Norway and the regional ethical committee to study the distribution and clearance of intrathecally injected gadobutrol by long-term, multiphase MRI in patients undergoing neurosurgical work-up of different CSF circulation disorders. As we reported in the AJNR, the intrathecal safety profile of gadobutrol was comparable with iodixanol, and the frequency of adverse events depended on the diagnosis.3
In several studies, we assessed the utility of gadobutrol as a CSF tracer. In patients with idiopathic normal pressure hydrocephalus (iNPH) dementia, who typically have histologic overlap with AD in brain specimens, we found a significantly reduced CSF molecular clearance rate compared with a younger reference cohort of patients with suspicion of CSF leaks, idiopathic intracranial hypertension, and cysts.4 From brain tissue, we also detected reduced molecular clearance from the entorhinal cortex, an area where atrophy is known to precede hippocampal degeneration in AD.5 From the hypothesis that brain molecular clearance of neurotoxic metabolites is impaired in the early symptomatic or even preclinical phase, we have suggested that the method may have the potential to diagnose reduced molecular clearance capacity before irreversible neurodegeneration has occurred.6