Involvement Of Posterior Cingulate Cortex Research Articles

Regional spectral ratios as potential neural markers to identify mild cognitive impairment related to Alzheimer's disease.

Alzheimer's disease (AD) has prolonged asymptomatic or mild symptomatic periods. Given that there is an increase in treatment options and that early intervention could modify the disease course, it is desirable to devise biological indices that may differentiate AD and nonAD at mild cognitive impairment (MCI) stage. Based on two well-acknowledged observations of background slowing (attenuation in alpha power and enhancement in theta and delta powers) and early involvement of posterior cingulate cortex (PCC, a neural hub of default-mode network), this study devised novel neural markers, namely, spectral ratios of alpha1 to delta and alpha1 to theta in the PCC. We analysed 46 MCI patients, with 22 ADMCI and 24 nonADMCI who were matched in age, education, and global cognitive capability. Concordant with the prediction, the regional spectral ratios were lower in the ADMCI group, suggesting its clinical application potential. Previous research has verified that neural markers derived from clinical electroencephalography may be informative in differentiating AD from other neurological conditions. We believe that the spectral ratios in the neural hubs that show early pathological changes can enrich the instrumental assessment of brain dysfunctions at the MCI (or pre-clinical) stage.

Involvement of posterior cingulate cortex in ketamine-induced psychosis relevant behaviors in rats

The involvement of posterior cingulate cortex (PCC) on ketamine-induced psychosis relevant behaviors was investigated in rats. Bilateral infusion of muscimol, a GABAA receptor agonist, into the PCC significantly antagonized ketamine-induced deficit in prepulse inhibition of a startle reflex (PPI), deficit in gating of hippocampal auditory evoked potentials, and behavioral hyperlocomotion in a dose dependent manner. Local infusion of ketamine directly into the PCC also induced a PPI deficit. Systemic injection of ketamine (3mg/kg,s.c.) induced an increase in power of electrographic activity in the gamma band (30–100Hz) in both the PCC and the hippocampus; peak theta (4–10Hz) power was not significantly altered, but peak theta frequency was increased by ketamine. In order to exclude volume conduction from the hippocampus to PCC, inactivation of the hippocampus was made by local infusion of muscimol into the hippocampus prior to ketamine administration. Muscimol in the hippocampus effectively blocked ketamine-induced increase of gamma power in the hippocampus but not in the PCC, suggesting independent generation of gamma waves in PCC and hippocampus. It is suggested that the PCC is part of the brain network mediating ketamine-induced psychosis related behaviors.

Brain correlates of risky decision-making

Understanding the neurocognitive basis of risk-taking behavior is an important issue, especially in economic decision-making. Classical behavioral studies have shown that risk-attitude changes across different contexts, but little is so far known about the brain correlates of processing of outcomes across such context shifts. In this study, EEG was recorded while subjects performed a gambling task. Participants could choose between a risky and a safer option, within two different contexts: one in which options yielded gains and losses of the same magnitude (Zero Expected Value context) and another in which gains were larger than losses (Positive Expected Value context). Based on their risk-attitude, two groups were compared: subjects who are risk-seekers in the zero Expected Value context (Zero-Oriented group) and subjects who are risk-seekers in the positive Expected Value condition (Positive-Oriented group). The Feedback Related Negativity (FRN) reflects this distinction, with each group being insensitive to magnitude of outcomes in the condition in which they were risk-prone. P300 amplitude mirrored the behavioral results, with larger amplitudes in the condition in which each group showed a higher risk-tendency. Source analyses highlighted the involvement of posterior cingulate cortex in risky decision-making. Taken together, the findings make a contribution to the clarification of the neurocognitive substrates of risky decision-making.