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Psychiatric disorders and related intermediate phenotypes are highly heritable and have a complex, overlapping polygenic architecture. A large-scale genome-wide association study (GWAS) of anxiety disorders identified genetic variants that are significant on a genome-wide. The current study investigated the genetic etiological overlaps between anxiety disorders and frequently cooccurring psychiatric disorders and intermediate phenotypes.
Using case–control and factor score models, we investigated the genetic correlations of anxiety disorders with eight psychiatric disorders and intermediate phenotypes [the volumes of seven subcortical brain regions, childhood cognition, general cognitive ability and personality traits (subjective well-being, loneliness, neuroticism and extraversion)] from large-scale GWASs (n = 7556–298 420) by linkage disequilibrium score regression.
Among psychiatric disorders, the risk of anxiety disorders was positively genetically correlated with the risks of major depressive disorder (MDD) (rg ± standard error = 0.83 ± 0.16, p = 1.97 × 10−7), schizophrenia (SCZ) (0.28 ± 0.09, p = 1.10 × 10−3) and attention-deficit/hyperactivity disorder (ADHD) (0.34 ± 0.13, p = 8.40 × 10−3). Among intermediate phenotypes, significant genetic correlations existed between the risk of anxiety disorders and neuroticism (0.81 ± 0.17, p = 1.30 × 10−6), subjective well-being (−0.73 ± 0.18, p = 4.89 × 10−5), general cognitive ability (−0.23 ± 0.08, p = 4.70 × 10−3) and putamen volume (−0.50 ± 0.18, p = 5.00 × 10−3). No other significant genetic correlations between anxiety disorders and psychiatric or intermediate phenotypes were observed (p > 0.05). The case–control model yielded stronger genetic effect sizes than the factor score model.
Our findings suggest that common genetic variants underlying the risk of anxiety disorders contribute to elevated risks of MDD, SCZ, ADHD and neuroticism and reduced quality of life, putamen volume and cognitive performance. We suggest that the comorbidity of anxiety disorders is partly explained by common genetic variants.
Depression and anxiety disorders (AD) are the first and sixth leading causes of disability worldwide. Despite their high prevalence and significant disability resulted, there are limited advances in new drug development. Recently, genome-wide association studies (GWAS) have greatly advanced our understanding of the genetic basis underlying psychiatric disorders.
Here we employed gene-set analyses of GWAS summary statistics for drug repositioning. We explored five related GWAS datasets, including two on major depressive disorder (MDD2018 and MDD-CONVERGE, with the latter focusing on severe melancholic depression), one on AD, and two on depressive symptoms and neuroticism in the population. We extracted gene-sets associated with each drug from DSigDB and examined their association with each GWAS phenotype. We also performed repositioning analyses on meta-analyzed GWAS data, integrating evidence from all related phenotypes.
Importantly, we showed that the repositioning hits are generally enriched for known psychiatric medications or those considered in clinical trials. Enrichment was seen for antidepressants and anxiolytics but also for antipsychotics. We also revealed new candidates or drug classes for repositioning, some of which were supported by experimental or clinical studies. For example, the top repositioning hit using meta-analyzed p values was fendiline, which was shown to produce antidepressant-like effects in mouse models by inhibition of acid sphingomyelinase.
Taken together, our findings suggest that human genomic data such as GWAS are useful in guiding drug discoveries for depression and AD.
The interaction of physical and mental vulnerability and environmental constraints is thought to foster the development of psychiatric disorders such as major depressive disorder (MDD). A central factor in the development of psychopathology is mental stress. Despite some evidence for parasympathetic withdrawal and sympathetic overactivity in MDD, the psychophysiological response to stress in depression is not clear-cut. Given the growing interest in heart rate and heart rate variability as indicators for remote monitoring of patients, it is important to understand how patients with MDD react to stress in a laboratory-controlled environment. We conducted a systematic review of studies using electrocardiography to derive heart rate and heart rate variability during stress in patients with clinical depression. We focused on well-validated stress tasks- the mental arithmetic stress task, the Trier social stress task and public speaking task- to minimize confounding effects due to the nature of the stressor. The majority of studies found hypo-reactivity during stress as a hallmark of depression as evidenced by lower fluctuation in heart rate and heart rate variability in the high-frequency band. We address the potential underlying biological mechanisms, the influence of covariates on these measures and briefly discuss the specificity and potential for remote monitoring by using these variables.
In this report we describe an 82-year female with a longstanding anxiety disorder who developed severe psychogenic dysphagia, leading to hospitalization due to failure to thrive. We describe for the first time the use of electroconvulsive therapy (ECT) to successfully manage a patient with pharmacological treatment resistant psychogenic dysphagia.
Identifying clinical features that predict conversion to bipolar disorder (BD) in those at high familial risk (HR) would assist in identifying a more focused population for early intervention.
In total 287 participants aged 12–30 (163 HR with a first-degree relative with BD and 124 controls (CONs)) were followed annually for a median of 5 years. We used the baseline presence of DSM-IV depressive, anxiety, behavioural and substance use disorders, as well as a constellation of specific depressive symptoms (as identified by the Probabilistic Approach to Bipolar Depression) to predict the subsequent development of hypo/manic episodes.
At baseline, HR participants were significantly more likely to report ⩾4 Probabilistic features (40.4%) when depressed than CONs (6.7%; p < .05). Nineteen HR subjects later developed either threshold (n = 8; 4.9%) or subthreshold (n = 11; 6.7%) hypo/mania. The presence of ⩾4 Probabilistic features was associated with a seven-fold increase in the risk of ‘conversion’ to threshold BD (hazard ratio = 6.9, p < .05) above and beyond the fourteen-fold increase in risk related to major depressive episodes (MDEs) per se (hazard ratio = 13.9, p < .05). Individual depressive features predicting conversion were psychomotor retardation and ⩾5 MDEs. Behavioural disorders only predicted conversion to subthreshold BD (hazard ratio = 5.23, p < .01), while anxiety and substance disorders did not predict either threshold or subthreshold hypo/mania.
This study suggests that specific depressive characteristics substantially increase the risk of young people at familial risk of BD going on to develop future hypo/manic episodes and may identify a more targeted HR population for the development of early intervention programs.
Altered amygdala activation to fear-related stimuli has been proposed to be a potential neural correlate of heightened threat sensitivity in anxiety- and stress-related disorders. However, the role of stimulus awareness and disorder specificity remains widely unclear. Here we investigated amygdala responses to conscious and unconscious fearful faces in patients suffering from panic disorder (PD), generalized anxiety disorder (GAD), or post-traumatic stress disorder (PTSD) and in a large sample of healthy controls (HC).
During event-related functional magnetic resonance imaging participants (n = 120; 20 PD, 20 GAD, 20 PTSD, 60 HC) were confronted with briefly presented fearful faces, neutral faces, and non-faces in a backward masking paradigm. The design allowed for the analysis of trial-by-trial face detection performance and amygdala responses to fearful v. neutral faces.
All participants exhibited increased amygdala activation to fearful v. neutral faces during conscious trials. Specifically during unconscious face processing, the PTSD, compared with all other groups, showed higher right basolateral (BLA) amygdala activity to fearful v. neutral faces.
The present study shows that BLA amygdala hyperactivity during unconscious, but not conscious, processing of fearful faces differentiates PTSD from the investigated disorders. This finding suggests an automatic and specific neural hyper-responsivity to general fear cues in PTSD and supports the idea of categorical differences between PTSD and other anxiety-related disorders.
Our aim was to examine the prevalence, correlates, and association of depressive and anxiety disorders with quality of life (QoL) and such other outcomes as the need for psychosocial services in cancer patients.
A total of 400 patients participated in a multicenter survey involving five cancer centers located throughout Korea. The Short-Form Health Survey, the MD Anderson Symptom Inventory, the Mini-Mental Adjustment to Cancer (MINI-MAC), and Mini-International Neuropsychiatric Interview were administered.
The prevalence rates for depressive and anxiety disorders were 16 and 17.1%, respectively. Younger age and poor Eastern Cooperative Oncology Group performance status, and all physical symptoms, as well as helplessness/hopelessness, anxious preoccupation (AP), and cognitive avoidance (CA) on the MINI-MAC were found to be significantly related to depressive disorder (DD) in a univariate logistic regression analysis. Metastases, the symptoms of disturbed sleep, dry mouth, and numbness or tingling, as well as AP and CA were significantly correlated with anxiety disorder (AD) in the univariate analysis. In the multivariate analyses, only AP was significant for AD (odds ratio = 2.94, p < 0.001), while none reached statistical significance for DD. Psychiatric comorbidity status had a detrimental effect on various dimensions of QoL. Patients with DD or AD reported a significantly higher need for professional psychosocial services.
Significance of results:
Given the substantial prevalence and pervasive impact of DD and AD on various aspects of QoL, its assessment and care should be integrated as a regular part of oncological care throughout the cancer continuum.
Depressive and anxiety disorders are associated with shorter leukocyte telomere length (LTL), an indicator of cellular aging. It is, however, unknown which pathways underlie this association. This study examined the extent to which lifestyle factors and physiological changes such as inflammatory or metabolic alterations mediate the relationship.
We applied mediation analysis techniques to data from 2750 participants of the Netherlands Study of Depression and Anxiety. LTL was assessed using quantitative polymerase chain reaction. Independent variables were current depressive (30-item Inventory of Depressive Symptoms – Self Report) and anxiety (21-item Beck's Anxiety Inventory) symptoms and presence of a depressive or anxiety disorder diagnosis based on DSM-IV; mediator variables included physiological stress systems, metabolic syndrome components and lifestyle factors.
Short LTL was associated with higher symptom severity (B = −2.4, p = 0.002) and current psychiatric diagnosis (B = −63.3, p = 0.024). C-reactive protein, interleukin-6, waist circumference, triglycerides, high-density lipoprotein cholesterol and cigarette smoking were significant mediators in the relationship between psychopathology and LTL. When all significant mediators were included in one model, the effect sizes of the relationships between LTL and symptom severity and current diagnosis were reduced by 36.7 and 32.7%, respectively, and the remaining direct effects were no longer significant.
Pro-inflammatory cytokines, metabolic alterations and cigarette smoking are important mediators of the association between depressive and anxiety disorders and LTL. This calls for future research on intervention programs that take into account lifestyle changes in mental health care settings.
Early intervention has become a priority for many researchers interested in reducing the prevalence of anxiety disorders within Australia (Donovan & Spence, 2000). Despite substantial advances in our knowledge of effective intervention protocols, studies investigating preventive intervention for child anxiety are sparse. Universal prevention programs targeting large cohorts of children within community settings are considered most advantageous (Greenburg, Domitrovich, & Bumbarger, 2001), although empirical studies for anxiety in youth are only beginning to emerge. This review of research in anxiety intervention explored protocols shown to have been successful in reducing symptoms of anxiety in youth and to discuss implications for future research. Findings suggested that cognitive behavioural therapy was potentially effective in reducing anxiety symptoms in youngsters when implemented in clinical settings (Kendall, 1994, 1996; Barrett, 1996, 1998) and in school-based preventive intervention (Dadds, Spence, Holland, Barrett, & Laurens, 1998). Future research evaluating the effectiveness of prevention programs at different ages in development has further practical research implications in terms of identifiing the most appropriate time conducive to enhancing long-term intervention effects.
Obsessive-compulsive disorder (OCD) is a chronic, relapsing mental illness. Selective serotonin reuptake inhibitors block serotonin transporters (SERTs) and are the mainstay of treatment for OCD. SERT abnormalities are reported in drug-free patients with OCD, but it is not known what happens to SERT levels during treatment. This is important as alterations in SERT levels in patients under treatment could underlie poor response, or relapse during or after treatment. The aim of the present study was first to validate a novel approach to measuring SERT levels in people taking treatment and then to investigate SERT binding potential (BP) using [11C]DASB PET in patients with OCD currently treated with escitalopram in comparison with healthy controls.
Twelve patients and age- and sex-matched healthy controls were enrolled. The patients and healthy controls underwent serial PET scans after administration of escitalopram and blood samples for drug concentrations were collected simultaneously with the scans. Drug-free BPs were obtained by using an inhibitory Emax model we developed previously.
The inhibitory Emax model was able to accurately predict drug-free SERT BP in people taking drug treatment. The drug-free BP in patients with OCD currently treated with escitalopram was significantly different from those in healthy volunteers [Cohen's d = 0.03 (caudate), 1.16 (putamen), 1.46 (thalamus), −5.67 (dorsal raphe nucleus)].
This result extends previous findings showing SERT abnormalities in drug-free patients with OCD by indicating that altered SERT availability is seen in OCD despite treatment. This could account for poor response and the high risk of relapse in OCD.
Despite the considerable physical, emotional and social change that occurs during emerging adulthood, there is little research that examines the association between having a chronic health condition and mental disorder during this developmental period. The aims of this study were to examine the sex-specific prevalence of lifetime mental disorder in an epidemiological sample of emerging adults aged 15–30 years with and without chronic health conditions; quantify the association between chronic health conditions and mental disorder, adjusting for sociodemographic and health factors; and, examine potential moderating and mediating effects of sex, level of disability and pain.
Data come from the Canadian Community Health Survey-Mental Health. Respondents were 15–30 years of age (n = 5947) and self-reported whether they had a chronic health condition. Chronic health conditions were classified as: respiratory, musculoskeletal/connective tissue, cardiovascular, neurological and endocrine/digestive. The World Health Organization Composite International Diagnostic Interview 3.0 was used to assess the presence of mental disorder (major depressive disorder, suicidal behaviour, bipolar disorder and generalised anxiety disorder).
Lifetime prevalence of mental disorder was significantly higher for individuals with chronic health conditions compared with healthy controls. Substantial heterogeneity in the prevalence of mental disorder was found in males, but not in females. Logistic regression models adjusting for several sociodemographic and health factors showed that the individuals with chronic health conditions were at elevated risk for mental disorder. There was no evidence that the level of disability or pain moderated the associations between chronic health conditions and mental disorder. Sex was found to moderate the association between musculoskeletal/connective tissue conditions and bipolar disorder (β = 1.71, p = 0.002). Exploratory analyses suggest that the levels of disability and pain mediate the association between chronic health conditions and mental disorder.
Physical and mental comorbidity is prevalent among emerging adults and this relationship is not augmented, but may be mediated, by the level of disability or pain. Findings point to the integration and coordination of public sectors – health, education and social services – to facilitate the prevention and reduction of mental disorder among emerging adults with chronic health conditions.
Substantial healthcare resources are devoted to panic disorder (PD) and coronary heart disease (CHD); however, the association between these conditions remains controversial. Our objective was to conduct a systematic review of studies assessing the association between PD, related syndromes, and incident CHD.
Relevant studies were retrieved from Medline, EMBASE, SCOPUS and PsycINFO without restrictions from inception to January 2015 supplemented with hand-searching. We included studies that reported hazard ratios (HR) or sufficient data to calculate the risk ratio and 95% confidence interval (CI) which were pooled using a random-effects model. Studies utilizing self-reported CHD were ineligible. Twelve studies were included comprising 1 131 612 persons and 58 111 incident CHD cases.
PD was associated with the primary incident CHD endpoint [adjusted HR (aHR) 1.47, 95% CI 1.24–1.74, p < 0.00001] even after excluding angina (aHR 1.49, 95% CI 1.22–1.81, p < 0.00001). High to moderate quality evidence suggested an association with incident major adverse cardiac events (MACE; aHR 1.40, 95% CI 1.16–1.69, p = 0.0004) and myocardial infarction (aHR 1.36, 95% CI 1.12–1.66, p = 0.002). The risk for CHD was significant after excluding depression (aHR 1.64, 95% CI 1.45–1.85) and after depression adjustment (aHR 1.38, 95% CI 1.03–1.87). Age, sex, length of follow-up, socioeconomic status and diabetes were sources of heterogeneity in the primary endpoint.
Meta-analysis showed that PD was independently associated with incident CHD, myocardial infarction and MACE; however, reverse causality cannot be ruled out and there was evidence of heterogeneity.
Twin studies of internalizing disorders suggest that their high co-morbidity is partially explained by shared genetic risk. Few studies have investigated pleiotropic effects of well-validated candidate genes across phenotypes.
Subjects were 928 Caucasian patients who presented to an out-patient clinic specializing in the assessment and treatment of anxiety and mood disorders. We constructed latent dimensional phenotypes across the internalizing spectrum (neuroticism, extraversion, depression, generalized anxiety, panic/agoraphobia, social phobia, post-traumatic stress, and obsessions–compulsions) by combining diagnostic criteria with other clinical indicators. We selected multiple variants in four evidence-based candidate genes (SLC6A4, COMT, GAD1, RGS2) with previously reported effects on several of these phenotypes. We conducted genetic association testing of their direct and indirect effects as well as gene × stress interactions (G × E).
We detected 19 nominally significant main effect associations for the 10 polymorphisms tested among the eight phenotypes (24%). These were generally phenotype non-specific, showing pleiotropic effects across multiple domains. The majority of observed sharing was between depression, panic disorder, and post-traumatic stress disorder. Some of these were best explained by mediational models in which genes increase liability for disorders indirectly via their effects on temperament. Limited G × E effects were detected between variants in SLC6A4 and both panic/agoraphobia and post-traumatic stress.
Examining just a few candidate genes for their potential roles in internalizing phenotypes, we found moderate support for the shared effects of several polymorphisms. These findings highlight the richness and complexity by which genes potentially contribute to psychopathology via pleiotropy, moderation by stress, and mediation by temperament.
Mental disorders in the elderly are common, with a 12-month prevalence in the community ranging from 8.54% to 26.4%. Unfortunately, many mental disorders are unrecognized, untreated, and associated with poor health outcomes. The aim of this paper is to describe the prevalence of mental disorders in the elderly primary care (PC) population and its associated factors by age groups.
Cross-sectional survey, conducted in 77 PC centers in Catalonia (Spain), 1,192 patients over 65 years old. The prevalence of mental disorders was assessed through face-to-face evaluations using the Structured Clinical Interview for DSM-IV Axis I Disorders, Research Version (SCID-I-RV) and the Mini International Neuropsychiatric Interview (MINI); chronic physical conditions were noted using a checklist; and disability through the Sheehan Disability Scales (SDS).
Nearly 20% of participants had a mental disorder in the previous 12 months. Anxiety disorders were the most frequent, (10.9%) (95% CI = 8.2–14.4), followed by mood disorders (7.4%) (95% CI = 5.7–9.5). Being female, greater perceived stress and having mental health/emotional problems as the main reason for consultation were associated with the presence of any mental disorder. There were no differences in prevalence across age groups. Somatic comorbidity was not associated with the presence of mental disorders.
Mental disorders are highly prevalent among the elderly in PC in Spain. Efforts are needed to develop strategies to reduce this prevalence and improve the well-being of the elderly. Based on our results, we thought it might be useful to assess perceived stress regularly in PC, focusing on people who consult for emotional distress, or that have greater perceived stress.
Background: Patients with anxiety disorder diagnoses commonly have more than one anxiety diagnosis. While cognitive-behavioural interventions have proven efficacy in treating single anxiety disorder diagnoses, there has been little investigation of their efficacy in treating co-occurring anxiety disorders. Aims: To evaluate the efficacy of a transdiagnostic cognitive-behavioural intervention for treating co-occurring anxiety disorders. Method: An A-B single case study design (N = 6) was used to evaluate the efficacy of a 12 to 13-session modular transdiagnostic cognitive-behavioural intervention for treating co-occurring anxiety disorders across patients with at least two of the following diagnoses: GAD, Social Phobia, Panic Disorder and/or OCD. Results: Five of the six participants completed treatment. At posttreatment assessment the five treatment completers achieved diagnostic and symptomatic change, with three participants being diagnosis free. All participants who completed treatment no longer met criteria for any DSM-IV-TR Axis-I diagnosis at the 3-month follow-up assessment, and demonstrated reliable and clinically-significant improvements in symptoms. Across the participants, statistically significant improvements from pre to postintervention were found on measures of anxiety, depression and general well-being, and all improvements were maintained at 3-month follow-up. Conclusions: Results suggest that transdiagnostic cognitive behavioural interventions can be of benefit to patients with co-occurring anxiety disorders.
The anxiety disorders are a prevalent mental health problem in older age with a considerable impact on quality of life. Until recently there have been few longitudinal studies on anxiety in this age group, consequently most of the evidence to date has been cross-sectional in nature.
We undertook a literature search of Medline, PsycINFO, the Cochrane trials database and the TRIP medical database to identify longitudinal studies which would help elucidate natural history and prognosis of anxiety disorders in the elderly.
We identified 12 papers of 10 longitudinal studies in our Review. This represented 34,691 older age participants with 5,199 with anxiety disorders including anxious depression and 3,532 individuals with depression without anxiety. Relapse rates of anxiety disorders are high over 6 year follow-up with considerable migration to mixed anxiety-depression and pure depressive mood episodes. Mixed anxiety-depression appears to be a poorer prognostic state than pure anxiety or pure depression with higher relapse rates across studies. In community settings treatment rates are low with 7–44% of the anxious elderly treated on antidepressant medications.
To our knowledge this is the first Systematic Review of longitudinal trials of anxiety disorders in older people. Major longitudinal studies of the anxious elderly are establishing the high risk of relapse and persistence alongside the progression to depression and anxiety depression states. There remains considerable under-treatment in community studies. Specialist assessment and treatment and major public health awareness of the challenges of anxiety disorders in the elderly are required.
An inherent prerequisite to mental health first-aid (MHFA) is the ability to identify that there is a mental health problem, but little is known about the association between psychiatric labelling and MHFA. This study examined this association using data from two national surveys of Australian young people.
This study involved a national telephonic survey of 3746 Australian youth aged 12–25 years in 2006, and a similar survey in 2011 with 3021 youth aged 15–25 years. In both surveys, respondents were presented with a vignette portraying depression, psychosis or social phobia in a young person. The 2011 survey also included depression with suicidal thoughts and post-traumatic stress disorder. Respondents were asked what they thought was wrong with the person, and reported on their first-aid intentions and beliefs, which were scored for quality of the responses.
Accurate labelling of the mental disorder was associated with more helpful first-aid intentions and beliefs across vignettes, except for the intention to listen non-judgementally in the psychosis vignette.
Findings suggest that community education programmes that improve accurate psychiatric label use may have the potential to improve the first-aid responses young people provide to their peers, although caution is required in the case of psychosis.
The aim of this study was to evaluate the validity of a new apathy rating scale in predicting the ability to return to work (RTW) in patients with depression or anxiety a year after discharge from a psychiatric hospital.
We evaluated 56 patients with depression or anxiety, who participated in an on-going randomised clinical trial using RTW as primary outcome. The degree of apathy was measured by the Diagnostic Apathia Scale, which contains six items covering the following neuropsychological symptoms: concentration/memory problems, difficulties in decision making, lassitude, tiredness/fatigue, insomnia, and reduced ability to work and engage in personal interests. The scale was analysed for psychometric validity (scalability) and for its ability to predict RTW. Finally, the predictive validity of the Diagnostic Apathia Scale regarding RTW was compared with scales measuring severity of depression/anxiety symptoms, disability, and psychological well-being.
The Diagnostic Apathia Scale displayed sufficient scalability, that is, the total score was a psychometrically valid measure of apathy. Only the Diagnostic Apathia Scale, and not the scales measuring severity of symptoms, disability, or psychological well-being, had predictive validity regarding RTW. Thus, 76% with ‘clinically significant apathy’ at baseline were unable to RTW versus 50% of the patients without apathy (p<0.05).
The Diagnostic Apathia Scale was found to have an acceptable predictive validity in terms of patients’ ability to RTW 1 year after discharge from hospitalisation for depression or anxiety.
The inability to inhibit certain behaviors is a key feature of impulsivity, which is often present in people with a substance use disorder. However, the findings on impulsivity in people with alcohol dependence (AD) are inconsistent, possibly because of the frequent co-occurrence of depression/anxiety (D/A) and its influence on impulsivity. In the current study, we aimed to distinguish response inhibition impairments in AD from possible response inhibition effects associated with D/A.
AD patients (n = 31) with high D/A co-morbidity were compared to patients with D/A only (n = 18) and healthy controls (HCs; n = 16) using the Stop Signal Task (SST) during functional magnetic resonance imaging (fMRI). Correlation analyses were performed between activated brain areas, behavioral data and addiction and D/A characteristics.
The three groups did not differ on response inhibition performance. However, AD severity, but not D/A severity, was positively associated with decreased response inhibition. During the SST, AD patients showed hyperactivity in the putamen and thalamus compared with D/A patients and HCs. Thalamus activation was negatively associated with AD duration. In addition, AD patients showed hypoactivity in the supplementary motor area (SMA) compared with HCs. SMA activity within HCs was negatively correlated with depressive symptom severity.
In general, AD patients were not more impulsive than D/A patients or HCs but they did reveal inhibition impairments with increasing AD severity. A shift from cortical to subcortical engagement in AD patients during response inhibition may represent an alternative strategy, which decreased with longer drinking history, suggesting the presence of an AD-specific endophenotype.