Area 31, which forms the caudal and dorsal-most part of the posterior cingulate cortex, occupies much of the cingulate sulcus when area 23c disappears (Fig. 1) and has even broader layers II IV (Vogt et al., 1987).
Degenerative neural cell bodies have been found within the hippocampus (CA3 region) and within the medial and lateral entorhinal cortex, and the cingulate cortex of adult rats with placental insufficiency.
Recently, thinning of the precuneus and posterior cingulate cortex (which includes the isthmus of the cingulate cortex) has been reported in adolescents diagnosed with ODD or CD (Fahim et al., 2011; Hyatt et al., 2012; Wallace et al., 2014).
9, 11 Degenerating axons were found within the corpus callosum, white matter of the cingulate cortex, somatosensory cortex, pontocerebellar tract, and the internal and external capsules.
It is well established that in sporadic AD the brain regions early and more severely affected are the medial temporal lobes, especially, the hippocampus and entorhinal cortex, the posterior portion of the cingulate gyrus, and the precuneus [ 66, 67].
Sixteen delay conditioning studies found activation of the ACC (e.g. [25], [26]), five of the posterior cingulate cortex (PCC) (e.g. [30]), and two reported activation of the cingulate cortex [33], [57].
It includes the prefrontal medial and superior frontal cortex, the posterior medial part of the cingulate gyrus and precuneus, and the bilateral inferior parietal cortex.
This includes large bilateral activations within the OFC, insula, cerebellum and parts of the cingulate cortex.
However, tracing studies in the monkey demonstrated that the posterior insula was connected to Brodmann areas 23 and 24 of the cingulate cortex [35], supporting our current findings.
In a recent work we also showed that chronic inflammatory pain related sensitization is mediated by the altered activation and connectivity of the cingulate cortex in rats [65].
