[1] Along with the precuneus, the PCC has been implicated as a neural substrate for human awareness in numerous studies of both the anesthetized and vegetative (coma) states.
As part of the paralimbic cortex, it has fewer than six layers, placing its cell architecture in between the six-layered neocortex and the more primitive allocortex of core limbic structures.
[5][7] The posterior cingulate cortex is highly connected and one of the most metabolically active regions in the brain, but there is no consensus as to its cognitive role.
[6] More recently the PCC was shown to display intense activity when autobiographical memories (such as those concerning friends and family) are recalled successfully.
In a study involving autobiographical recollection, the caudal part of the left PCC was the only brain structure highly active in all subjects.
[6] The posterior cingulate cortex is significantly bilaterally activated by emotional stimuli, independent of valence (positive or negative).
The default mode network (and the PCC) is highly reactive and quickly deactivates during tasks with externally directed, or presently centered, attention (such as working memory or meditation).
[4][8] Conversely, the DMN is active when attention is internally directed (during episodic memory retrieval, planning, and daydreaming).
A failure of the DMN to deactivate at proper times is associated with poor cognitive function, thereby indicating its importance in attention.
[4] Considering the relation of the PCC with the DMN, with suppressed posterior cingulate activity favoring low cognitive introspection and higher external attention and increased activity indicating memory retrieval and planning, it has been hypothesized that this brain region is heavily involved in noticing internal and external changes and in facilitating novel behavior or thought in response.
[5] An alternative hypothesis is focused more on the difference between the dorsal and ventral subregions and takes into consideration their functional separation.
In this model, the PCC is hypothesized to take a chief regulatory role in focusing internal and external attention.
Mounting evidence that the PCC is involved in both integrating memories of experiences and initiating a signal to change behavioral strategies supports this hypothesis.
[4] While both of the hypotheses are the result of scientific studies, the role of the PCC is still not well understood and there remains much work to be done to investigate the extent of their veracity.
[15] In fact, reduced metabolism in the PCC has been identified as an early sign of Alzheimer's disease, and is frequently present before a clinical diagnosis.
[16] In Alzheimer's disease, metabolic abnormality is linked to amyloid deposition and brain atrophy with a spatial distribution that resembles the nodes of the default mode network.
[4] This transmission of abnormal protein would be constrained by the organization of white matter connections and could potentially explain the spatial distribution of pathology within the DMN, in Alzheimer's .
[4] Finally, post-mortem studies show that the PCC in patients with ASD have cytoarchitectonic abnormalities, including reduced levels of GABA A receptors and benzodiazepine binding sites.
[4] It has been suggested that ADHD is a disorder of the DMN, where neural systems are disrupted by uncontrolled activity that leads to attentional lapses.
Furthermore, patients who undergo deep brain stimulation, have increased glucose metabolism and cerebral flow in the PCC, while also showing an altered Brodmann area 25.
[4] Abnormal activity in the PCC has been linked to schizophrenia, a mental disorder with common symptoms such as hallucinations, delusions, disorganized thinking, and a lack of emotional intelligence.
They also found that greater damage to the cingulum bundle, that connects the PCC to the anterior DMN, was correlated with sustained attention impairment.
[35] Within selected tasks, patients with TBI showed impaired motor inhibition that was associated with failure to rapidly reactive the PCC.