the back, more flattened part of the
cingulate cortex, a structure in the forebrain that forms a collar around the
corpus callosum. Like the
anterior cingulate cortex, the PCC also is divided into two sections, referred to as the
dorsal posterior cingulate cortex (
dPCC) and the
ventral posterior cingulate cortex (
vPCC), respectively. Although its precise characteristics and mechanisms are not yet fully understood, the PCC has been shown to play a role in numerous processes, including
episodic memory,
spatial attention,
preattentive processing, sensory processing (
visual processing,
auditory processing, etc.),
sensory integration, motor intention, emotional responses, and self-reflection and other self-referential processing. Additionally, it is a key component of the
limbic system and forms part of the recently identified
default-mode network, a set of specific brain regions whose activity predominates in the resting state and is inhibited during cognitively demanding and externally cued perceptual tasks. Structural and functional alterations of the PCC appear to underlie several disorders, including Alzheimer’s disease, autism spectrum disorder, depression, dyslexia, and schizophrenia. For example, several studies have revealed atrophy and decreased metabolic activity (hypometabolism)—particularly of the enzyme
cytochrome oxidase—within the PCC of individuals who display
mild cognitive impairment and subsequently develop Alzheimer’s disease, as well as reduced connectivity between the PCC, hippocampus, and other brain regions.