Recognition Deficits Research Articles

Affective prosody disorders in adults with neurological conditions: A scoping review.

Individuals with affective-prosodic deficits have difficulty understanding or expressing emotions and attitudes through prosody. Affective prosody disorders can occur in multiple neurological conditions, but the limited knowledge about the clinical groups prone to deficits complicates their identification in clinical settings. Additionally, the nature of the disturbance underlying affective prosody disorder observed in different neurological conditions remains poorly understood. To bridge these knowledge gaps and provide relevant information to speech-language pathologists for the management of affective prosody disorders, this study provides an overview of research findings on affective-prosodic deficits in adults with neurological conditions by answering two questions: (1) Which clinical groups present with acquired affective prosodic impairments following brain damage? (2) Which aspects of affective prosody comprehension and production are negatively affected in these neurological conditions? We conducted a scoping review following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses Extension for Scoping Reviews guidelines. A literature search was undertaken in five electronic databases (MEDLINE, PsycINFO, EMBASE, CINAHL and Linguistics, and Language Behavior Abstracts) to identify primary studies reporting affective prosody disorders in adults with neurological impairments. We extracted data on clinical groups and characterised their deficits based on the assessment task used. The review of 98 studies identified affective-prosodic deficits in 17 neurological conditions. The task paradigms typically used in affective prosody research (discrimination, recognition, cross-modal integration, production on request, imitation and spontaneous production) do not target the processes underlying affective prosody comprehension and production. Therefore, based on the current state of knowledge, it is not possible to establish the level of processing at which impairment occurs in clinical groups. Nevertheless, deficits in the comprehension of affective prosody are observed in 14 clinical groups (mainly recognition deficits) and deficits in the production of affective prosody (either on request or spontaneously) in 10 clinical groups. Neurological conditions and types of deficits that have not been investigated in many studies are highlighted. The aim of this scoping review was to provide an overview on acquired affective prosody disorders and to identify gaps in knowledge that warrant further investigation. Deficits in the comprehension or production of affective prosody are common to numerous clinical groups with various neurological conditions. However, the underlying cause of affective prosody disorders across them is still unknown. Future studies should implement standardised assessment methods with specific tasks based on a cognitive model to identify the underlying deficits of affective prosody disorders. What is already known on the subject What is already known on the subjectAffective prosody is used to share emotions and attitudes through speech and plays a fundamental role in communication and social interactions. Affective prosody disorders can occur in various neurological conditions, but the limited knowledge about the clinical groups prone to affective-prosodic deficits and about the characteristics of different phenotypes of affective prosody disorders complicates their identification in clinical settings. Distinct abilities underlying the comprehension and production of affective prosody can be selectively impaired by brain damage, but the nature of the disturbance underlying affective prosody disorders in different neurological conditions remains unclear. What this study adds Affective-prosodic deficits are reported in 17 neurological conditions, despite being recognised as a core feature of the clinical profile in only a few of them. The assessment tasks typically used in affective prosody research do not provide accurate information about the specific neurocognitive processes impaired in the comprehension or production of affective prosody. Future studies should implement assessment methods based on a cognitive approach to identify underlying deficits. The assessment of cognitive/executive dysfunctions, motor speech impairment and aphasia might be important for distinguishing primary affective prosodic dysfunctions from those secondarily impacting affective prosody. What are the potential clinical implications of this study? Raising awareness about the possible presence of affective-prosodic disorders in numerous clinical groups will facilitate their recognition by speech-language pathologists and, consequently, their management in clinical settings. A comprehensive assessment covering multiple affective-prosodic skills could highlight specific aspects of affective prosody that warrant clinical intervention.

Long-term Memory Testing in Children With Typical Development and Neurodevelopmental Disorders: Remote Web-based Image Task Feasibility Study.

Neurodevelopmental disorders (NDD) cause individuals to have difficulty in learning facts, procedures, or social skills. NDD has been linked to several genes, and several animal models have been used to identify potential therapeutic candidates based on specific learning paradigms for long-term and associative memory. In individuals with NDD, however, such testing has not been used so far, resulting in a gap in translating preclinical results to clinical practice. We aim to assess if individuals with NDD could be tested for paired association learning and long-term memory deficit, as shown in previous animal models. We developed an image-based paired association task, which can be performed at different time points using remote web-based testing, and evaluated its feasibility in children with typical development (TD), as well as NDD. We included 2 tasks: object recognition as a simpler task and paired association. Learning was tested immediately after training and also the next day for long-term memory. We found that children aged 5-14 years with TD (n=128) and with NDD of different types (n=57) could complete testing using the Memory Game. Children with NDD showed deficits in both recognition and paired association tasks on the first day of learning, in both 5-9-year old (P<.001 and P=.01, respectively) and 10-14-year old groups (P=.001 and P<.001, respectively). The reaction times to stimuli showed no significant difference between individuals with TD or NDD. Children with NDD exhibited a faster 24-hour memory decay for the recognition task than those with TD in the 5-9-year old group. This trend is reversed for the paired association task. Interestingly, we found that children with NDD had their retention for recognition improved and matched with typically developing individuals by 10-14 years of age. The NDD group also showed improved retention deficits in the paired association task at 10-14 years of age compared to the TD group. We showed that web-based learning testing using simple picture association is feasible for children with TD, as well as with NDD. We showed how web-based testing allows us to train children to learn the association between pictures, as shown in immediate test results and those completed 1 day after. This is important as many models for learning deficits in NDD target both short- and long-term memory for therapeutic intervention. We also demonstrated that despite potential confounding factors, such as self-reported diagnosis bias, technical issues, and varied participation, the Memory Game shows significant differences between typically developing children and those with NDD. Future experiments will leverage this potential of web-based testing for larger cohorts and cross-validation with other clinical or preclinical cognitive tasks.

Verbal memory formation across PET-based Braak stages of tau accumulation in Alzheimer's disease.

A classical early sign of typical Alzheimer's disease is memory decline, which has been linked to the aggregation of tau in the medial temporal lobe. Verbal delayed free recall and recognition tests have consistently probed useful to detect early memory decline, and there is substantial debate on how performance, particularly in recognition tests, is differentially affected through health and disease in older adults. Using in vivo PET-Braak staging, we investigated delayed recall and recognition memory dysfunction across the Alzheimer's disease spectrum. Our cross-sectional study included 144 cognitively unimpaired elderly, 39 amyloid-β+ individuals with mild cognitive impairment and 29 amyloid-β+ Alzheimer's disease patients from the Translational Biomarkers in Aging and Dementia cohort, who underwent [18F]MK6240 tau and [18F]AZD4694 amyloid PET imaging, structural MRI and memory assessments. We applied non-parametric comparisons, correlation analyses, regression models and voxel-wise analyses. In comparison with PET-Braak Stage 0, we found that reduced, but not clinically significant, delayed recall starts at PET-Braak Stage II (adjusted P < 0.0015), and that recognition (adjusted P = 0.011) displayed a significant decline starting at PET-Braak Stage IV. While performance in both delayed recall and recognition related to tau in nearly the same cortical areas, further analyses showed that delayed recall rendered stronger associations in areas of early tau accumulation, whereas recognition displayed stronger correlations in mostly posterior neocortical regions. Our results support the notion that delayed recall and recognition deficits are predominantly associated with tau load in allocortical and neocortical areas, respectively. Overall, delayed recall seems to be more dependent on the integrity of anterior medial temporal lobe structures, while recognition appears to be more affected by tau accumulation in cortices beyond medial temporal regions.

Contrasting Metacognitive, Emotion Recognition and Alexithymia Profiles in Bulimia, Anorexia, and Schizophrenia.

Alexithymia, or deficits in emotion recognition, and metacognitive capacity have been noted both in psychosis and eating disorders and potentially linked to psychopathology. This study sought to compare levels of impairments in these phenomena and their associations with psychopathology in groups with eating disorders and psychosis. Participants with diagnoses of a schizophrenia spectrum disorder (SSD; n = 53), anorexia (n = 40), or bulimia (n = 40) were recruited from outpatient clinics. Alexithymia was measured with the Toronto Alexithymia Scale; emotion recognition, with the Ekman Faces Test; and metacognition, with the Metacognitive Assessment Scale-Abbreviated. Psychopathology was measured with the Eating Attitudes Test, Body Image Questionnaire, and Positive and Negative Syndrome Scale. Results indicated that the SSD group had significantly poorer metacognitive function than either eating disorder group. Metacognition was related to body image in the anorexia group and a range of different forms of general psychopathology in the bulimia group. Alexithymia was related to eating disorder behaviors in the bulimia group.

Comparisons of facial emotion recognition in different social contexts among patients with schizophrenia, major depressive disorder and bipolar disorder.

Previous studies have found that patients with schizophrenia (SCZ), major depressive disorder (MDD), and bipolar disorder (BD) all have facial emotion recognition deficits, but the differences and similarities of these deficits in the three groups of patients under different social interaction situations are not clear. The present study aims to compare the ability of facial emotion recognition in three different conversation situations from a cross-diagnostic perspective. Thirty-three participants with SCZ, 35 participants with MDD, and 30 participants with BD were recruited, along with 31 healthy controls. A computer-based task was given to assess the ability of Facial Emotion Categorization (FEC) under three different conversational situations (praise, blame, and inquiry). In the "praise" situation, patients with SCZ, MDD and BD were all slower to recognize anger emotion than the healthy controls. In all three clinical groups, patients with SCZ recognized angry faces faster than those with MDD and BD on a continuum from happy faces to angry faces in the "inquiry" situation, while no significant difference was found in the latter two groups. In addition, no significant defect was found in the percentage and threshold of angry face recognition in all three patient groups. Our findings indicate that patients with SCZ, MDD, and BD share both common and distinct deficits in facial emotion recognition during social interactions, which may be beneficial for early screening and precise intervention for these mental disorders.

Probiotic Therapy with Lactobacillus reuteri Rescues Social and Emotional Recognition Behavior in an Environmental Mouse Model of Autism

Introduction: Polybrominated diphenyl ethers (PBDEs) are neuroendocrine disrupting chemicals with adverse neurodevelopmental effects in children. Our group has previously shown that PBDEs produce autistic-like traits in developmentally exposed mice offspring (Kozlova et al. 2022 Arch Tox; PMID: 34687351). Our pilot data suggests that PBDEs reduce hypothalamic oxytocin expression. Moreover, PBDEs are well established disruptors of thyroid hormones. Lactobacillus reuteri (LR) is a beneficial probiotic that can increase oxytocin and thyroid hormones in other ASD mouse models. Therefore, we hypothesized that LR can restore PBDE-induced deficits in social behavior. Methods: C57BL/6N dams were dosed with a commercial mixture of PBDE congeners, DE-71, at 0.1 mg/kg/d (DE-71), or corn oil vehicle control (VEH/CON) for 10 wk (preconception: 4 wk; gestation: 3 wk; lactation: 3 wk). Dams were gavaged with L. reuteri (LR) ATCC 6475 (gift of Biogaia, Sweeden) at 10 8 CFU/mL. Cohort 1 pups (C1-LR) received LR via dam until weaning (PND 21). Cohort 2 pups (C2-LR) continued to receive gavage of LR post-weaning, daily, through 6 mo of age. Results: PCR analysis showed increased gene expression of fecal LR 6475 in feces collected from LR offspring and dams confirming efficacy of maternal LR supplementation. Compared to VEH/CON neither DE-71 nor LR disrupted normal maternal behavior. In offspring, DE-71 produced deficient short- (SRT, 30 min retention) and long-term social recognition memory (SRMT, 24 h retention) in adult females (short- and long-term) and adult males (short-term). LR normalized these deficits. The social recognition deficit was not present at PND 11 as measured on a maternal attachment homing test. On an emotional recognition test DE-71 exposed male and female offspring did not prefer investigation of stimulus mice subjected to 15 min restraint stress vs neutral conditions (normalized with LR). In a marble burying test, compared to VEH/CON, DE-71 exposed offspring showed abnormally elevated scores, which were normalized by LR treatment only in females. Developmental benchmarks that are likely affected by the TH-disruptive effects of DE-71 showed complex interactions between DE-71 and LR. LR normalized delayed (vs VEH/CON) incisor eruption in DE-71 females and improved latency of righting reflex in DE-71 males. LR normalized DE-71-induced hyperactivity on an open field test in females. Ongoing studies are focused on exploring possible mechanisms underlying the normalization provided by LR. However, our early data suggest a potential role of 1) OXT confirmed by increased plasma OXT in DE-71 male (C1-LR) mice and normalized with LR, and 2) maternal THs since LR supplementation elevated plasma T4 in DE-71 pregnant dams. Conclusions: These results suggest that maternal LR treatment during developmental PBDE exposure provides normalization of autistic-like features in a sex-dependent manner. This work is supported by a Danone North America Gut Microbiome, Yogurt and Probiotics Fellowship Grant and a University of California President's Pre-Professoriate Fellowship to E.V.K. This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Autism Spectrum Disorder and Face Identity Recognition Deficit across Ages

The purpose of this review was to assess the face identity recognition deficit and the developmental difference that manifested in autism spectrum disorder (ASD) compared to their typically developing (TD) peers. Based on the meta-analysis using a random-effect model of 94 studies, with 144 effect sizes, for both adult and pediatric subjects with simultaneous and delayed face identity recognition paradigms, the underperformance in ASD was significant and persistent across ages. In addition, a higher level of deficit was found in adult ASD when performing simultaneous face-matching tasks while other subgroups showed homogenous effect sizes. This suggested a dissociation between the difficulties of the two mechanisms of face recognition: face perception (perceiving identity from the face with minimal memory load required) and face memory (recall of identity from the face that requires memory load), which was only shown in adults but not in children. The result indicated the possibility of using face identity recognition deficit as a diagnostic trait for ASD.

Establishing the relationship between ADHD and emotional facial expression recognition deficit: a systematic review (P1-12.005)

Establishing the relationship between ADHD and emotional facial expression recognition deficit: a systematic review (P1-12.005)

Social Cognition in Opioid Use Disorder

Background: Opioid use disorder (OUD) is associated with significant functional impairment and neurocognitive dysfunction, but only a handful of studies have investigated social cognitive abilities in this condition. This study aimed to investigate facial emotion recognition accuracy/biases and two different aspects of theory of mind (ToM) (ToM-decoding vs ToM-reasoning) in people with recovered OUD. Methods: The participants included 32 people with recovered OUD who were on Buprenorphine + Naloxone (B/N) maintenance treatment and 32 healthy controls. In addition to neurocognitive tasks, both groups were assessed by a facial emotion recognition task, the faux pas recognition task, and the reading the mind from the eyes task. Results: In comparison to healthy controls, people on B/N maintenance treatment showed deficits in facial emotion recognition (d = 1.32) and both aspects of ToM (d = 0.87–1.21). In analyses of individual emotions, people on B/N maintenance treatment had decreased accuracy in recognition of anger and fear and had a bias to identify other emotions as sad. The duration of opioid use was robustly associated with difficulties in the recognition of anger. Conclusion: People in B/N maintenance treatment have significant difficulties in recognizing the emotions and mental states of others. Deficits in social cognition might be important for understanding the difficulties in interpersonal and social functioning in people with OUD.

What is the prevalence of developmental prosopagnosia? An empirical assessment of different diagnostic cutoffs.

The prevalence of developmental prosopagnosia (DP), lifelong face recognition deficits, is widely reported to be 2-2.5%. However, DP has been diagnosed in different ways across studies, resulting in differing prevalence rates. In the current investigation, we estimated the range of DP prevalence by administering well-validated objective and subjective face recognition measures to an unselected web-based sample of 3116 18-55 year-olds and applying DP diagnostic cutoffs from the last 14 years. We found estimated prevalence rates ranged from .64-5.42% when using a z-score approach and .13-2.95% when using a percentile approach, with the most commonly used cutoffs by researchers having a prevalence rate of .93% (z-score, .45% when using percentiles). We next used multiple cluster analyses to examine whether there was a natural grouping of poorer face recognizers but failed to find consistent grouping beyond those with generally above versus below average face recognition. Lastly, we investigated whether DP studies with more relaxed diagnostic cutoffs were associated with better performance on the Cambridge Face Perception Test. In a sample of 43 studies, there was a weak nonsignificant association between greater diagnostic strictness and better DP face perception accuracy (Kendall's tau-b correlation, τb=.18 z-score; τb=.11 percentiles). Together, these results suggest that researchers have used more conservative DP diagnostic cutoffs than the widely reported 2-2.5% prevalence. We discuss the strengths and weaknesses of using more inclusive cutoffs, such as identifying mild and major forms of DP based on DSM-5.

EXPRESS: Recognition of facial expressions in autism: effects of face masks and alexithymia.

It is often assumed that the recognition of facial expressions is impaired in autism. However, recent evidence suggests that reports of expression recognition difficulties in autistic participants may be attributable to co-occurring alexithymia - a trait associated with difficulties interpreting interoceptive and emotional states - not autism per se. Due to problems fixating on the eye-region, autistic individuals may be more reliant on information from the mouth region when judging facial expressions. As such, it may be easier to detect expression recognition deficits attributable to autism, not alexithymia, when participants are forced to base expression judgements on the eye-region alone. To test this possibility, we compared the ability of autistic participants (with and without high levels of alexithymia) and non-autistic controls to categorize facial expressions i) when the whole face was visible, and ii) when the lower portion of the face was covered with a surgical mask. High-alexithymic autistic participants showed clear evidence of expression recognition difficulties: they correctly categorised fewer expressions than non-autistic controls. In contrast, low-alexithymic autistic participants were unimpaired relative to non-autistic controls. The same pattern of results was seen when judging masked and unmasked expression stimuli. In sum, we find no evidence for an expression recognition deficit attributable to autism, in the absence of high levels of co-occurring alexithymia, either when participants judge whole-face stimuli or just the eye-region. These findings underscore the influence of co-occurring alexithymia on expression recognition in autism.

The Relationship between Motor Symptoms, Signs, and Parkinsonism with Facial Emotion Recognition Deficits in Individuals with 22q11.2 Deletion Syndrome at High Genetic Risk for Psychosis

Background. The 22q11.2 Deletion Syndrome (22q11.2DS) is a genetic condition at high risk of developing both psychosis and motor disorders. Social Cognition (SC) deficits have been associated not only with schizophrenia but also with Parkinson’s disease (PD). The present study assessed SC deficits in 22q11.2DS and investigated the interaction between motor symptoms and deficits in Facial Emotion Expressions (FEE) recognition and in Theory of Mind (ToM) tasks in people with 22q11.2DS. Methods. We recruited 38 individuals with 22q11.2DS without psychosis ( N = 38 , DEL) and 18 with 22q11.2DS and psychosis ( N = 18 , DEL_SCZ). The Positive And Negative Syndrome Scale (PANSS), Ekman’s 60 Faces Test (EK-60F), the Awareness of Social Inference Test (TASIT EmRec), and the Movement Disorder Society-Unified Parkinson’s Disease Rating Scale part III (UPDRS III) were administered. Correlations were sought between UPDRS III and both TASIT EmRec and EK-60F scores. Analyses were conducted separately for each psychopathological subgroup. Results. Higher UPDRS III ( p = 0.04 ) and lower EK-60F ( p = 0.025 ) scores were observed in the DEL_SCZ group. We found inverse correlations between UPDRS III and both TASIT EmRec ( r = − 0.289 , p = 0.031 ) and EK-60F ( r = − 0.387 , p = 0.006 ) scores in the whole sample. Correlations were no longer significant in the DEL_SCZ group (UPDRS III-TASIT EmRec p = 0.629 ; UPDRS III-EK60F p = 0.933 ) whilst being stronger in the DEL group (TASIT EmRec, r = − 0.560 , p &lt; 0.001 ; EK60F, r = − 0.542 , p &lt; 0.001 ). Analyses were adjusted for CPZ Eq and IQ. Conclusions. A modulation between FEE recognition deficits and motor symptoms and signs was observed in the 22q11.2DS group, likely affecting patients’ quality of life.

Thinking versus feeling: How interoception and cognition influence emotion recognition in behavioural-variant frontotemporal dementia, Alzheimer's disease, and Parkinson's disease

Disease-specific mechanisms underlying emotion recognition difficulties in behavioural-variant frontotemporal dementia (bvFTD), Alzheimer's disease (AD), and Parkinson's disease (PD) are unknown. Interoceptive accuracy, accurately detecting internal cues (e.g., one's heart beating), and cognitive abilities are candidate mechanisms underlying emotion recognition.One hundred and sixty-eight participants (52 bvFTD; 41 AD; 24 PD; 51 controls) were recruited. Emotion recognition was measured via the Facial Affect Selection Task or the Mini-Social and Emotional Assessment Emotion Recognition Task. Interoception was assessed with a heartbeat detection task. Participants pressed a button each time they: 1) felt their heartbeat (Interoception); or 2) heard a recorded heartbeat (Exteroception-control). Cognition was measured via the Addenbrooke's Cognitive Examination-III or the Montreal Cognitive Assessment. Voxel-based morphometry analyses identified neural correlates associated with emotion recognition and interoceptive accuracy.All patient groups showed worse emotion recognition and cognition than controls (all P's ≤ .008). Only the bvFTD showed worse interoceptive accuracy than controls (P < .001). Regression analyses revealed that in bvFTD worse interoceptive accuracy predicted worse emotion recognition (P = .008). Whereas worse cognition predicted worse emotion recognition overall (P < .001). Neuroimaging analyses revealed that the insula, orbitofrontal cortex, and amygdala were involved in emotion recognition and interoceptive accuracy in bvFTD.Here, we provide evidence for disease-specific mechanisms for emotion recognition difficulties. In bvFTD, emotion recognition impairment is driven by inaccurate perception of the internal milieu. Whereas, in AD and PD, cognitive impairment likely underlies emotion recognition deficits. The current study furthers our theoretical understanding of emotion and highlights the need for targeted interventions.

Facial emotion recognition deficits in schizophrenia - a review of research and a model of pathogenesis

Objective: The aim of the paper is to describe in detail the problems in the field of recognising emotional facial expressions in patients with schizophrenia. This paper also analyses studies and theoretical literature on the potential connections between deficits in recognition of emotional facial expressions and neuronal dysfunctions and attachment styles. Materials and method: The literature review was performed using the following databases: EBSCO, PsycINFO, PubMed, and Google Scholar. The databases were searched using the following keywords: ‘emotion’, ‘facial emotion’, ‘facial expression’. Those terms were combined with the words 'recognition', 'perception', 'genetic', 'attachment style' and each time with the term 'schizophrenia'. Results: The literature review clearly confirms that among people suffering from schizophrenia there are problems with recognising emotional facial expressions. Studies suggest that the visual perception of patients is related to the recognition of facial expressions. Studies also confirm the relationship of neuronal dysfunctions and genetic factors with the recognition of emotional facial expressions. Discussion and conclusions: The genesis of problems in recognising emotional facial expressions in patients with schizophrenia is multifactorial in nature. The influence of attachment styles on epigenetic mechanisms and the development of neural structures related to emotion recognition remains unverified. In the future, this study will allow for the creation of more accurate models of the pathogenesis of these deficits.

Emotion recognition of faces and emoji in individuals with moderate-severe traumatic brain injury

ABSTRACT Background Facial emotion recognition deficits are common after moderate-severe traumatic brain injury (TBI) and linked to poor social outcomes. We examine whether emotion recognition deficits extend to facial expressions depicted by emoji. Methods Fifty-one individuals with moderate-severe TBI (25 female) and fifty-one neurotypical peers (26 female) viewed photos of human faces and emoji. Participants selected the best-fitting label from a set of basic emotions (anger, disgust, fear, sadness, neutral, surprise, happy) or social emotions (embarrassed, remorseful, anxious, neutral, flirting, confident, proud). Results We analyzed the likelihood of correctly labeling an emotion by group (neurotypical, TBI), stimulus condition (basic faces, basic emoji, social emoji), sex (female, male), and their interactions. Participants with TBI did not significantly differ from neurotypical peers in overall emotion labeling accuracy. Both groups had poorer labeling accuracy for emoji compared to faces. Participants with TBI (but not neurotypical peers) had poorer accuracy for labeling social emotions depicted by emoji compared to basic emotions depicted by emoji. There were no effects of participant sex. Discussion Because emotion representation is more ambiguous in emoji than human faces, studying emoji use and perception in TBI is an important consideration for understanding functional communication and social participation after brain injury.

Potential Anti-Amnesic Activity of a Novel Multimodal Derivative of Salicylamide, JJGW08, in Mice.

Memory impairments constitute a significant problem worldwide, and the COVID-19 pandemic dramatically increased the prevalence of cognitive deficits. Patients with cognitive deficits, specifically memory disturbances, have underlying comorbid conditions such as schizophrenia, anxiety, or depression. Moreover, the available treatment options have unsatisfactory effectiveness. Therefore, there is a need to search for novel procognitive and anti-amnesic drugs with additional pharmacological activity. One of the important therapeutic targets involved in the modulation of learning and memory processes are serotonin receptors, including 5-HT1A, 5-HT6, and 5-HT7, which also play a role in the pathophysiology of depression. Therefore, this study aimed to assess the anti-amnesic and antidepressant-like potential of JJGW08, a novel arylpiperazine alkyl derivative of salicylamide with strong antagonistic properties at 5-HT1A and D2 receptors and weak at 5-HT2A and 5-HT7 receptors in rodents. First, we investigated the compound's affinity for 5-HT6 receptors using the radioligand assays. Next, we assessed the influence of the compound on long-term emotional and recognition memory. Further, we evaluated whether the compound could protect against MK-801-induced cognitive impairments. Finally, we determined the potential antidepressant-like activity of the tested compound. We found that JJGW08 possessed no affinity for 5-HT6 receptors. Furthermore, JJGW08 protected mice against MK-801-induced recognition and emotional memory deficits but showed no antidepressant-like effects in rodents. Therefore, our preliminary study may suggest that blocking serotonin receptors, especially 5-HT1A and 5-HT7, might be beneficial in treating cognitive impairments, but it requires further investigation.

(2R,6R)-Hydroxynorketamine Treatment of Rats Exposed to Repetitive Low-Level Blast Injury.

Many military veterans who experienced blast-related traumatic brain injuries (TBIs) in the conflicts in Iraq and Afghanistan suffer from chronic cognitive and mental health problems, including post-traumatic stress disorder (PTSD). Male rats subjected to repetitive low-level blast exposure develop chronic cognitive and PTSD-related traits that develop in a delayed manner. Ketamine has received attention as a treatment for refractory depression and PTSD. (2R,6R)-hydroxynorketamine [(2R,6R)-HNK] is a ketamine metabolite that exerts rapid antidepressant actions. (2R,6R)-HNK has become of clinical interest because of its favorable side-effect profile, low abuse potential, and oral route of administration. We treated three cohorts of blast-exposed rats with (2R,6R)-HNK, beginning 7-11 months after blast exposure, a time when the behavioral phenotype is established. Each cohort consisted of groups (n = 10-13/group) as follows: 1) Sham-exposed treated with saline, 2) blast-exposed treated with saline, and 3) blast-exposed treated with a single dose of 20 mg/kg of (2R,6R)-HNK. (2R,6R)-HNK rescued blast-induced deficits in novel object recognition (NOR) and anxiety-related features in the elevated zero maze (EZM) in all three cohorts. Exaggerated acoustic startle was reversed in cohort 1, but not in cohort 3. (2R,6R)-HNK effects were still present in the EZM 12 days after administration in cohort 1 and 27 days after administration in NOR testing of cohorts 2 and 3. (2R,6R)-HNK may be beneficial for the neurobehavioral syndromes that follow blast exposure in military veterans. Additional studies will be needed to determine whether higher doses or more extended treatment regimens may be more effective.

Cerebellar dysfunction and autism spectrum disorders – what do we know?

IntroductionAutism spectrum disorders (ASD) are complex neurodevelopmental conditions characterized by impairments in social cognition and repetitive behaviors with onset in early infancy. Deficits in emotion recognition, social perception, and communication have been identified as core symptoms of ASD.Comorbid disorders are frequent, namely psychiatric illness, epilepsy, sleep disruption, and hyperactivity.Immune profile changes during early life may contribute to pathogenesis of ASD. Other risk factors include advanced parental age, fetal environment, fertility treatments, medications, and nutritional and toxic factors.Several brain regions are involved in the pathophysiology of ASD but the cerebellum is the structure most consistently found altered. An increased risk of ASD is associated with cerebellar damage.ObjectivesTo highlight the importance of understanding the key processes of cerebellar development and how altered cerebellar function leads to social and cognitive impairments, and consequently ASD.MethodsNon-systematic review of the literature using Pubmed database. Papers were selected according to their relevance.ResultsFrom imaging studies, we can understand that cerebellum is not just about motor function. Different tasks like adding working memory, emotional and social processing, and language seem to be part of core functions of the cerebellar circuit.Adults with lesions in the cerebellum can develop cerebellar cognitive affective syndrome (CCAS), with core symptoms of impaired executive function, difficulties in spatial cognition, blunted affect, or inappropriate behavior. Some children who have tumor resection surgery for medulloblastomas also exhibit symptoms of CCAS, and some experience posterior fossa syndrome (PFS).The linguistic, cognitive, and behavioral deficits in CCAS and PFS may contribute to explaining how cerebellar alterations are related to ASD, which is a neurodevelopmental disorder characterized by an earlier onset and broader spectrum of these symptoms.ConclusionsThe literature has suggested an important role for cerebellar dysfunction in etiology of ASD, under certain premises: (a) cerebellar expansion temporarily coincides with onset of ASD; (b) cerebellum is prone to lesions during this period; (3) cerebellar lesions contribute to dysfunctional social and language abilities.Disturbances in cerebellar development lead to alterations in higher cognitive functions, due to changes in Purkinje cells. These dysfunctional neurons, once integrated into a brain circuit that controls complex tasks, lead to these functions becoming aberrant.It is therefore fair to say that cerebellum is important for development of the so-called “cognitive and social brain” since it is itself part of this network. So, the cerebellum certainly plays a relevant role in pathophysiology of ASD.Disclosure of InterestNone Declared

Emotional Recognition Training Enhances Attention to Emotional Stimuli Among Male Juvenile Delinquents.

Juvenile delinquents have deficits in emotional recognition that might play a critical role in the development of aggression. The present study aimed to investigate the effect of emotional recognition training and its consequences on emotional attention and aggression. Seventy-three male juvenile delinquents were randomly assigned to two groups. One group was the modification group, which received eight days of training on an emotional recognition task. The purpose of the training was to modify interpretative biases in emotion recognition to encourage the perception of happiness over anger in ambiguous expressions. The other group was the waitlist group, which did not perform a task and continued with their usual programme. Before and after the training, participants completed the aggression questionnaire (AQ) and two behavioural tasks, including the emotional recognition task and a visual search task with happy and angry faces as targets. The modification group recognized more faces as happy after emotional recognition training than the waitlist group. Furthermore, the hostility in the modification group decreased significantly. Importantly, emotional recognition training further affected attention to emotional faces as participants responded faster in searching for happy and angry faces after training. Emotional recognition training could modify juvenile delinquents' emotional recognition, enhance their visual attention to emotional faces and reduce hostility.

Examining the association between speed-accuracy trade-offs and psychopathy among male offenders in a facial affect recognition task.

Despite a large body of work examining the relationship between facial affect recognition and psychopathy, there is little consensus regarding the nature of emotion processing in such individuals. Although most previous studies have reported an association between psychopathy and some facial affect recognition deficits, results are mixed regarding which specific emotions are related to deficient recognition for these individuals. The current study aims to examine speed-accuracy trade-offs in psychopathy. Participants were 139 incarcerated adult male offenders assessed using the Psychopathy Checklist-Revised. Analyses demonstrated a 3-way interaction between psychopathy, response time, and level of stimulus expression for happiness in which psychopathy mitigated the relationship between response time and level of expression on accuracy. However, the overall pattern of findings does not suggest that speed-accuracy trade-offs are a central component of facial affect recognition in psychopathy. The theoretical implications of current findings are discussed. (PsycInfo Database Record (c) 2023 APA, all rights reserved).