We quantified rhythmic brain activity, recorded with whole-scalp magnetoencephalography (MEG), of 13 healthy subjects who were performing, seeing, or hearing the tapping of a drum membrane with the right index finger. In the actor's primary motor (M1) cortex, the level of the ≈20-Hz brain rhythms started to decrease, as a sign of M1 activation, ≈2 s before the action and then increased, with a clear rebound ≈0.6 s after the tapping, as a sign of M1 stabilization. A very similar time course occurred in the M1 cortex of the observer: the activation, although less vigorous than in the actor, started ≈0.8 s before the action and was followed by a rebound. When the subject just heard the tapping sound, no preaction activation was visible, but a rebound followed the sound. The ≈10-Hz somatosensory rhythm, which also started to decrease before own and viewed actions, returned to the baseline level ≈0.6 s later after own actions than observed actions. This delay likely reflects proprioceptive input to the cortex, available only during own actions, and therefore could be related to the brain signature of the sense of agency. The strikingly similar motor cortex reactivity during the first and third person actions expands previous data on brain mechanisms of intersubjective understanding. Besides motor cortex activation before own and observed (predicted) actions, the M1 cortex of both the viewer and the listener stabilized in a very similar manner after brisk motor actions.

Auditory and vibrotactile stimuli share similar temporal patterns. A psychophysical experiment was performed to test whether this similarity would lead into an intermodal bias in perception of sound intensity. Nine normal-hearing subjects performed a loudness-matching task of faint tones, adjusting the probe tone to sound equally loud as a reference tone. The task was performed both when the subjects were touching and when they were not touching a tube that vibrated simultaneously with the probe tone. The subjects chose on average 12% lower intensities $\text{(p<0.01)}$ for the probe tone when they touched the tube, suggesting facilitatory interaction between auditory and tactile senses in normal-hearing subjects.

Background: Adipose tissue dysfunction has been implicated in the pathophysiology of Alzheimer’s disease. However, the involvement of adipokines, particularly adiponectin, remains unclear. Objective: To compare serum and cerebrospinal fluid (CSF) levels of adiponectin, leptin and leptin-to-adiponectin ratio in patients within the spectrum of Alzheimer’s disease and evaluate their relationship with classical biomarkers and their value as markers of progression. Methods: Amnestic mild cognitive impairment (MCI, n = 71) and Alzheimer’s dementia (AD, n = 53) subjects were consecutively recruited for serum and CSF adiponectin and leptin determination using an analytically validated commercial enzyme-linked immunosorbent assay (ELISA). Correlations were explored using adjusted Spearman’s correlation coefficients. A logistic regression model and ROC analysis were performed to evaluate the staging predictive value of adipokines. Results: Serum adiponectin was 33% higher in AD when compared to MCI patients. Adiponectin CSF levels, similar in both groups, were positively correlated with A β ₄₂ and cognitive function, though only in women. The area under the ROC curve was 0.673 (95% CI:0.57-0.78) for serum adiponectin as predictor of dementia stage and the cut-off 10.85 μg/ml maximized the sum of specificity (87%) and sensitivity (44%). Conclusion: Although longitudinal studies are required, we hypothesize that higher serum adiponectin in AD patients constitutes a strategy to compensate possible central signaling defects. In addition, adiponectin might be specifically assigned to neuroprotective functions in women and eventually involved in the female-biased incidence of Alzheimer’s disease.