The Role of Metacognition in Pathological Gambling: A Mediation Model.

Pathological gambling involves multitudinous costs related to financial, legal, and public health care aspects, as well as to specific psychological disorders. Despite the overall evidence suggesting that comorbid disorders represent a risk factor for pathological gambling, there is scant evidence on the appropriate treatments for gamblers with such disorders. In this context, metacognitive therapy is an interesting approach because it considers psychological disorders as a result of the activation of perseverative cognitive processes and attentional strategies in response to inner events. Several studies report that metacognition is associated with different psychological problems. This study investigated the relationship among comorbid disorders, metacognition, and pathological gambling. 69 pathological gamblers at the first hospital admission and 58 controls drawn from general population (matched for age, gender, education) completed a battery of self report instruments: Symptom Checklist-90-R, Metacognition Questionnaire 30, South Oaks Gambling Scale. Compared to controls, pathological gamblers showed higher level of comorbid symptomatology and metacognition. Correlation analyses showed that: comorbid symptomatology and metacognition were positively and significantly correlated with pathological gambling; metacognition was positively and significantly associated with comorbid symptomatology. Mediation analysis indicated that dysfunctional metacognitive strategies could have an indirect effect on pathological gambling mediated by concurrent psychological disorders. These findings provide some implications for gambling treatment programs: pathological gamblers should be screened for psychiatric disorders, and metacognitive therapy could be considered a correct treatment of pathological gamblers. Metacognitive therapy might lead to the reduction of the pathological gambling by the diminishing of the concurrent psychological disorders.

[Correlation between cognitive impairment and plasma levels of clusterin/ApoJ in Parkinson disease patients not affected by dementia]. / Correlazione tra deterioramento cognitivo e livello plasmatico della clusterina/ApoJ in pazienti con malattia di Parkinson non affetti da demenza.

Cognitive impairment is frequent in patients with Parkinson's disease (PD), and can range from mild deterioration to dementia. Recently a contribution of Alzheimer's disease for the cognitive dysfunction in PD has been proposed, whereas the presence of tau protein and amyloid was recognized. Clusterin/ApoJ is a protein involved in the deposition of beta-amyloid and in its neurotoxicity. In this study we aimed to investigate the clusterin/ApoJ's plasma levels in patients with PD to assess its potential role in fisiopathogenetic cognitive impairment.

Midbrain SERT in degenerative parkinsonisms: a 123I-FP-CIT SPECT study.

SPECT imaging is widely used for the differential diagnosis of degenerative parkinsonisms by exploiting the high affinitiy of the radiotracer (123)I-FP-CIT for the dopamine transporter. Reduced levels of DAT are found in Parkinson Disease (PD), Dementia with Lewy Bodies (DLB), and Progressive Supranuclear Palsy (PSP) compared to in Essential Tremor (ET) and Healthy Controls (HC). However, the extent of the neurodegenerative process may extend beyond nigrostriatal system. We have exploited the affinity of the same radiotracer (123)I-FP-CIT for the serotonin transporter to investigate SERT levels in the midbrain of patients with PD, DLB, PSP, and ET compared to HC. Using MRI images as anatomical templates for midbrain uptake quantification, we found a mild decrease in SERT levels in PD compared to ET and HC, with marked inter-individual variability; on the other side, PSP and DLB patients displayed markedly reduced to undetectable levels of SERT, respectively. These findings show that the neurodegenerative process affects serotoninergic neurons in parkinsonisms, with much more severe involvement in DLB than in PD patients, despite the comparable loss of striatal DAT. SERT-dependent (123)I-FP-CIT uptake may allow a more comprehensive assessment of neurochemical disturbances in degenerative parkinsonisms and may have a value for differential diagnosis.

Severity of neuropsychiatric symptoms and dopamine transporter levels in dementia with Lewy bodies: a 123I-FP-CIT SPECT study.

Neuropsychiatric symptoms are frequent in dementia with Lewy bodies (DLB). Dopamine transporter (DAT) imaging with (123)I-labeled ligand N-delta-(fluoropropyl)-2 beta-carbomethoxy-3beta-(4-iodophenyl)tropene ((123)I-FP-CIT), which reliably measures midbrain dopaminergic dysfunction, has provided important evidence on the neurobiological substrate of some of these symptoms including apathy and depression. However, little is known on DAT levels and other distressing symptoms such as delusions and hallucinations. Therefore, (123)I-FP-CIT imaging was performed in 18 well-characterized patients with DLB, and striatal DAT levels were correlated with the frequency/severity ratings of several neuropsychiatric symptoms. A wide range of neuropsychiatric symptoms could be observed in the sample. Significant correlations were observed between decreased striatal DAT levels and visual hallucinations. Although there were no correlations between striatal DAT levels and other neuropsychiatric symptoms, when considering the putamen and the caudate nucleus separately, delusions, depression, and apathy were inversely correlated to decreased caudate DAT levels. The seresults provide intriguing evidence on the involvement of the mesocortical dopaminergic pathways in neuropsychiatric symptoms in DLB.