No abstract

Methamphetamine is a popular addictive drug whose use is associated with multiple neuropsychiatric adverse events and toxic to the dopaminergic and serotonergic systems of the brain. Methamphetamine-induced neuropathology is associated with increased expression of microglial cells that are thought to participate in either pro-toxic or protective mechanisms in the brain. Although reactive microgliosis has been observed in animal models of methamphetamine neurotoxicity, no study has reported on the status of microglial activation in human methamphetamine abusers. The present study reports on 12 abstinent methamphetamine abusers and 12 age-, gender-, and education-matched control subjects who underwent positron emission tomography using a radiotracer for activated microglia, [ C](R)-(1-[2-chlorophenyl]-N-methyl-N-[1-methylpropyl]-3-isoquinoline carboxamide) ([ C](R)-PK11195). Compartment analysis was used to estimate quantitative levels of binding potentials of [ C](R)-PK11195 in brain regions with dopaminergic and/or serotonergic innervation. The mean levels of [11 C](R)-PK11195 binding were higher in methamphetamine abusers than those in control subjects in all brain regions (Ͼ250% higher; p Ͻ 0.01 for all). In addition, the binding levels in the midbrain, striatum, thalamus, and orbitofrontal and insular cortices ( p Ͻ 0.05) correlated inversely with the duration of methamphetamine abstinence. These results suggest that chronic self-administration of methamphetamine can cause reactive microgliosis in the brains of human methamphetamine abusers, a level of activation that appears to subside over longer periods of abstinence.

The brains of autistic individuals have abnormalities in both serotonin transporter and dopamine transporter binding. The present findings indicate that the gross abnormalities in these neurotransmitter systems may underpin the neurophysiologic mechanism of autism. Our sample was not characteristic or representative of a typical sample of adults with autism in the community.

The present study suggests that an abnormality in glutamatergic neurotransmission may play a role in the pathophysiology of autism.

A lack of coupling between microglial activation and amyloid deposits may indicate that Aβ accumulation shown by [(11)C]PIB is not always the primary cause of microglial activation, but rather the negative correlation present in the PCC suggests that microglia can show higher activation during the production of Aβ in early AD.

Empathy cultivates deeper interpersonal relationships and is important for socialization. However, frequent exposure to emotionally-demanding situations may put people at risk for burnout. Burnout has become a pervasive problem among medical professionals because occupational burnout may be highly sensitive to empathy levels. To better understand empathy-induced burnout among medical professionals, exploring the relationship between burnout severity and strength of empathy-related brain activity may be key. However, to our knowledge, this relationship has not yet been explored. We studied the relationship between self-reported burnout severity scores and psychological measures of empathic disposition, emotional dissonance and alexithymia in medical professionals to test two contradictory hypotheses: Burnout is explained by (1) ‘compassion fatigue' that is, individuals become emotionally over involved; and (2) ‘emotional dissonance' that is, a gap between felt and expressed emotion, together with reduced emotional regulation. Then, we tested whether increased or decreased empathy-related brain activity measured by fMRI was associated with burnout severity scores and psychological measures. The results showed that burnout severity of medical professionals is explained by ‘reduced' empathy-related brain activity. Moreover, this reduced brain activity is correlated with stronger emotional dissonance and alexithymia scores and also greater empathic disposition. We speculate that reduced emotion recognition (that is, alexithymia) might potentially link with stronger emotional dissonance and greater burnout severity alongside empathy-related brain activity. In this view, greater empathic disposition in individuals with higher burnout levels might be due to greater difficulty identifying their own emotional reactions. Our study sheds new light on the ability to predict empathy-induced burnout.

Our aim is to investigate the neural substrates for writing using fMRI (twenty right-handed subjects). We assumed that common areas involved in both writing with right and left hands are crucial to the central process of writing. We employed Japanese phonograms (Kana), in which phoneme-grapheme conversion would be extremely simple. Brain activation was examined under three conditions: (1) written naming with the right hand (WR), (2) written naming with the left hand (WL), and (3) naming silently (NA). While the comparison of WR to NA (WR>NA) exhibited activation only in the left frontoparietal area, the WL>NA comparison exhibited broader activation than the WR>NA comparison, i.e., the left frontoparietal area except the motor and sensory areas and the right frontoparietal area. A conjunction analysis in SPM2 revealed common areas of activation across the WR>NA and WL>NA comparisons, which are assumed to be crucial to writing. In the group analysis, three areas were found to be activated: the posterior end of the left superior frontal gyrus, which is superior and posterior to Exner's center; the anterior part of the left superior parietal lobule; and the lower part of the anterior limb of the left supramarginal gyrus. In the single-subject analysis, whereas the first two of the above three areas were found to be crucial for writing in all individuals, an interindividual inconsistency of involvement with writing was observed in three areas: the lower part of the anterior limb of the left supramarginal gyrus (60% involved); the right frontal region (47%); and the right intraparietal sulcus (47%).

These findings suggest that decreased levels of TGF-beta1 may be implicated in the pathophysiology of autism.