Imaging neuronal loss and recovery in compromised but viable brain tissue

Abstract

Selective neuronal loss, that is necrosis or apoptosis of a portion of neurons in cerebral tissue with grossly preserved architecture (Garcia et al ., 1996), is difficult to assess but can seriously impact brain function in patients with cerebrovascular disease. It has been associated with temporary cerebral ischaemia, as in reperfused penumbral tissue (Garcia et al ., 1996; Baron, 2005), and with chronic cerebral hypoperfusion due, for example, to atherosclerotic disease of major cerebral arteries or ischaemic heart disease (Yamauchi et al ., 2011). Selective neuronal loss may be a significant factor in cognitive impairment and limited functional recovery ability. Conventional diagnostic imaging with CT or MRI does not identify selective neuronal damage (Garcia et al ., 1996; Sicard et al ., 2006). Peri-infarct tissue that displays normalization of T2 relaxation time on magnetic resonance images chronically after experimental transient cerebral ischaemia—reflective of oedema resolution—has been shown to contain areas with selective neuronal necrosis (Wegener et al ., 2006). On the other hand, single photon emission computed tomography (SPECT) with 123I-labelled iomazenil, or PET with 11C-labelled flumazenil, have the potential to detect tissue with selective neuronal loss and distinguish this from fully infarcted tissue (Hatazawa and Shimosegawa, 1998). The ligands iomazenil and flumazenil bind to central-type benzodiazepine receptors and reduced binding therefore reflects neuronal injury in cerebral …