OBJECTIVE: Despite several studies that have highlighted the harmful effects of alcohol consumption on cognitive functions it remains unclear whether certain brain areas are more sensitive than others are or whether alcohol causes widespread cognitive deficit. Moreover, the role of continued abstinence has yet to be clarified regarding the quality of recovery on the different cognitive domains. The aim of this 1-year longitudinal study was to evaluate the recovery of cognitive deficits in the medium (6 months) and long term (12 months) after the interruption of drinking. METHODS: Forty-one alcohol-dependent patients were recruited from two outpatient treatment facilities and cognitive functions were compared on a control group of forty healthy controls. The patients were then re-assessed at 6 and 12 months. Changes in neuropsychological measures were evaluated with repeated measures analysis of variance (ANOVA). We also compared 1-year follow-up scores with control data (unpaired t tests) to identify tests on which significant differences persisted. RESULTS: Patients performed significantly worse than controls in all cognitive domains investigated and this cognitive impairment was evident in recently abstinent patients. A year of abstinence resulted in a significant improvement in all cognitive domains assessed after detoxification from alcohol. After year 1, alcoholic subjects had returned to normal levels compared to healthy controls on all domains except for general non-verbal intelligence, verbal memory and some visuospatial skills. CONCLUSION: Our results support the hypothesis of widespread impairment resulting from alcohol consumption. The recovery of cognitive functions is not homogeneous during prolonged abstinence.
Alcohol Drinking ; Alcoholics ; Brain ; Cognition ; Cognition Disorders ; Drinking ; Follow-Up Studies ; Humans ; Intelligence ; Longitudinal Studies* ; Memory ; Outpatients

OBJECTIVE: The present study aims at exploring associations between a continuous measure of distorted thought contents and a set of demographic and clinical features in a sample of unipolar/bipolar depressed patients. METHODS: Our sample included 1,833 depressed subjects. Severity of mood symptoms was assessed by the 21 items Hamilton Depression Rating Scale (HAM-D). The continuous outcome measure was represented by a delusion (DEL) factor, extracted from HAM-D items and including items: 2 ("Feelings of guilt"), 15 ("Hypochondriasis"), and 20 ("Paranoid symptoms"). Each socio-demographic and clinical variable was tested by a generalized linear model test, having depressive severity (HAM-D score-DEL score) as the covariate. RESULTS: A family history of major depressive disorder (MDD; p=0.0006), a diagnosis of bipolar disorder, type I ( p=0.0003), a comorbid general anxiety disorder (p<0.0001), and a higher number of manic episodes during lifetime (p<0.0001), were all associated to higher DEL scores. Conversely, an older age at onset (p<0.0001) and a longer duration of hospitalization for depression over lifetime (p=0.0003) had a negative impact over DEL scores. On secondary analyses, only the presence of psychotic features (p<0.0001) and depressive severity (p<0.0001) were found to be independently associated to higher DEL scores. CONCLUSION: The retrospective design and a non validated continuous measure for distorted thought contents were the main limitations of our study. Excluding the presence of psychotic features and depressive severity, no socio-demographic or clinical variable was found to be associated to our continuous measure of distorted thinking in depression.
Anxiety Disorders ; Bipolar Disorder ; Delusions* ; Depression* ; Depressive Disorder, Major ; Diagnosis ; Hospitalization ; Humans ; Linear Models ; Outcome Assessment (Health Care) ; Psychotic Disorders ; Retrospective Studies ; Thinking

Objective: Genetic variations in the gene encoding zinc finger protein 804A gene (ZNF804A) have been associated with major depression and bipolar disorder. In this work we focused on the potential influence of ZNF804A variations on the risk of developing specific sub-phenotypes as well as the individual response to available treatments. Methods: We used two samples of different ethnic origin: a Korean sample, composed by 242 patients diagnosed with major depression and 132 patients diagnosed with bipolar disorder and 326 healthy controls; an Italian sample composed 151 major depression subjects, 189 bipolar disorder subjects and 38 outpatients diagnosed for a primary anxiety disorder. Results: Our analyses reported an association of rs1344706 with psychotic phenotype in the cross-diagnostic pooled sample (geno p = 4.15 × 10−4, allelic p = 1.06 × 10−4). In the cross-diagnosis Italian sample but not in the Korean one, rs7597593 was involved with depressive symptoms improvement after treatment (geno p = 0.025, allelic p = 0.007). Conclusion The present study evidenced the role of ZNF804A alterations in symptoms improvement after treatment. Both manic and depressive symptoms seem to be modulated by ZNF804A, though the latter was observed in the bipolar pooled sample only. The role of this factor is likely related to synaptic development and maintenance; however, further analyses will be needed to better understand the molecular mechanics involved with ZNF804A.