flexibility and renewed learning. 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. Under this model, the PCC plays a crucial role in controlling state of arousal, the breadth of focus and the internal or external focus of attention. This hypothesis emphasizes the PCC as a dynamic network, rather than a fixed and unchanging structure. 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. Meditation From neuroimaging studies and subjective descriptions, the PCC has been found to be activated during self-related thinking and deactivated during meditation. Using generative topographic mapping, it was further found that undistracted, effortless mind wandering corresponds with PCC deactivation, whereas distracted and controlled awareness corresponds with PCC activation. These results track closely with findings about the role of the PCC in the DMN. Disorders Structural and functional abnormalities in the PCC result in a range of neurological and psychiatric disorders. The PCC likely integrates and mediates information in the brain. Therefore, functional abnormalities of the PCC might be an accumulation of remote and widespread damage in the brain. Alzheimer's disease The PCC is commonly affected by neurodegenerative disease. 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. The reduced metabolism in the PCC is typically one part in a diffuse pattern of metabolic dysfunction in the brain that includes medial temporal lobe structures and the anterior thalamus, abnormalities that may be the result of damage in isolated but connected regions. For instance, Meguro et al. (1999) show that experimental damage of the rhinal cortex results in hypometabolism of the PCC. 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. In early Alzheimer's, functional connectivity within the DMN is reduced, affecting the connection between the PCC and the hippocampus, and these