Pathological Behavior Research Articles

Lesions of uncertain malignant potential in breast: Role of multiparametric MRI and histopathological correlation

Objectives This study aims to retrospectively evaluate the role of multiparametric magnetic resonance imaging (MRI), including diffusion-weighted imaging (DWI) with apparent diffusion coefficient (ADC) mapping, in predicting the histopathological upgrade of B3 breast lesions. The primary objective is to calculate the mean ADC values for B3 and B5 lesions. The secondary objective involves evaluating the kinetic enhancement patterns of these lesions. Materials and Methods This retrospective analysis includes patients who underwent MR mammography between 2019 and 2023 in our institution and subsequently underwent trucut biopsy and histopathologically proven to be either B3 or B5 category breast lesions. Results Student’s t-test was used to find out the significant difference in ADC between the two groups. B5 lesions had lower mean ADC value (0.8 ± 0.2 ×10–3 mm2/sec, p = 0.026), whereas B3 lesions had higher mean ADC value (1.1 ± 0.3 × 10–3 mm2/sec, p = 0.026). Conclusion The multiparametric MRI including DWI in high-risk breast lesions would help in predicting their pathological behavior non-invasively. Identifying the mean ADC value and MR morphological characteristics in these lesions may guide clinicians in reducing misdiagnosis and over-treatment.

Fecal Microbiota Transplantation (FMT) From a Human at Low Risk for Alzheimer's Disease Improves Short-Term Recognition Memory and Increases Neuroinflammation in a 3xTg AD Mouse Model.

Human microbiota-associated murine models, using fecal microbiota transplantation (FMT) from human donors, help explore the microbiome's role in diseases like Alzheimer's disease (AD). This study examines how gut bacteria from donors with protective factors against AD influence behavior and brain pathology in an AD mouse model. Female 3xTgAD mice received weekly FMT for 2 months from (i) an 80-year-old AD patient (AD-FMT), (ii) a cognitively healthy 73-year-old with the protective APOEe2 allele (APOEe2-FMT), (iii) a 22-year-old healthy donor (Young-FMT), and (iv) untreated mice (Mice-FMT). Behavioral assessments included novel object recognition (NOR), Y-maze, open-field, and elevated plus maze tests; brain pathology (amyloid and tau), neuroinflammation (in situ autoradiography of the 18 kDa translocator protein in the hippocampus); and gut microbiota were analyzed. APOEe2-FMT improved short-term memory in the NOR test compared to AD-FMT, without significant changes in other behavioral tests. This was associated with increased neuroinflammation in the hippocampus, but no effect was detected on brain amyloidosis and tauopathy. Specific genera, such as Parabacteroides and Prevotellaceae_UGC001, were enriched in the APOEe2-FMT group and associated with neuroinflammation, while genera like Desulfovibrio were reduced and linked to decreased neuroinflammation. Gut microbiota from a donor with a protective factor against AD improved short-term memory and induced neuroinflammation in regions strategic to AD. The association of several genera with neuroinflammation in the APOEe2-FMT group suggests a collegial effect of the transplanted microbiome rather than a single-microbe driver effect. These data support an association between gut bacteria, glial cell activation, and cognitive function in AD.

Schizophrenia-related Xpo7 haploinsufficiency leads to behavioral and nuclear transport pathologies.

Recent genetic studies by the Schizophrenia Exome Sequencing Meta-Analysis (SCHEMA) consortium have identified that protein-truncating variants of exportin 7 (XPO7) can increase the risk of schizophrenia (odds ratio, 28.1). Here we show that mice with Xpo7 haploinsufficiency (Xpo7+/- mice) present with cognitive and social behavioral impairments. Through proteome analysis using immunoprecipitation and frontal cortex nuclear isolation of Xpo7+/- mice, we identify 45 molecules interacting with Xpo7, including CutC, Rbfox3, and Gria3. Through single-nucleus RNA sequencing of the frontal cortex and striatum of Xpo7+/- mice differentiating between the onset and progressive stages, we also identify 284 gene expression changes that correlate with these stages. These genes encompass high-odds risk genes of schizophrenia identified by SCHEMA, including Gria3, Grin2A, Herc1, and Trio. Furthermore, our approach reveals 15 gene expression changes in the frontal cortex that correlate with the progressive stages. Our findings indicate the importance of investigating whether the interactions among the high-risk genes identified by SCHEMA contribute to a common schizophrenia pathology and underscore the significance of stage-dependent analysis.

Cannabinoid type-1 receptors in CaMKII neurons drive impulsivity in pathological eating behavior.

Overconsumption of palatable food and energy accumulation are evolutionary mechanisms of survival when food is scarce. This innate mechanism becomes detrimental in obesogenic environment promoting obesity and related comorbidities, including mood disorders. The endocannabinoid system favors energy accumulation and regulates reward circuits. We applied a genetic strategy to reconstitute cannabinoid type-1 receptor (CB1) expression at functional levels specifically in CaMKII+neurons (CaMKII-CB1-RS) and adipocytes (Ati-CB1-RS), respectively, in a CB1 deficient background. Rescued CB1 expression in CaMKII+neurons, but not in adipocytes, promotes feeding behavior, leading to fasting-induced hyperphagia, increased motivation, and impulsivity to palatable food seeking. In a diet-induced obesity model, CB1 re-expression in CaMKII+neurons, but not in adipocytes, compared to complete CB1 deficiency, was sufficient to largely restore weight gain, food intake without any effect on glucose intolerance associated with high-fat diet consumption. In a model of glucocorticoid-mediated metabolic syndrome, CaMKII-CB1-RS mice showed all metabolic alterations linked to the human metabolic syndrome except of glucose intolerance. In a binge-eating model mimicking human pathological feeding, CaMKII-CB1-RS mice showed increased seeking and compulsive behavior to palatable food, suggesting crucial roles in foraging and an enhanced susceptibility to addictive-like eating behaviors. Importantly, other contingent behaviors, including increased cognitive flexibility and reduced anxiety-like behaviors, but not depressive-like behaviors, were also observed. To sum up, CB1 in CaMKII+neurons is instrumental in feeding behavior and energy storage under physiological conditions. The exposure to risk factors (hypercaloric diet, glucocorticoid dysregulation) leads to obesity, metabolic syndrome, binge-eating and food addiction.

Forsythoside B Ameliorates Neuroinflammation via Inhibiting NLRP3 Inflammasome of Glial Cells in Experimental Autoimmune Encephalomyelitis Mice.

Neuroinflammation mediated by glial cells plays a crucial role in demyelination in experimental autoimmune encephalomyelitis (EAE), a multiple sclerosis (MS) model. Forsythoside B (FTS·B), a natural phenylethanoid glycoside isolated from the dried fruits and leaves of Forsythia suspensa (Thunb.) Vahl, has been found to have antioxidant, anti-apoptotic, and anti-inflammatory properties. However, there is currently no report or research on the effectiveness of FTS·B treatment for EAE. The aim of this study was to investigate the neuroprotective properties of (FTS·B) on EAE and reveal its potential mechanisms. Myelin oligodendrocyte glycoprotein-induced EAE mice were randomly categorized into the control, EAE model, and FTS·B treatment groups. Behavioral testing, pathology, immunohistochemistry, immunofluorescence staining, and western blot analysis of spinal cord tissue were used to determine the effects and mechanisms of FTS·B on EAE in mice. We found that FTS·B treatment could significantly alleviate and reduce the clinical symptoms and morbidity of EAE, respectively. In addition, FTS·B administration reduced inflammatory response and demyelination by inhibiting glial cell activation in the spinal cord of EAE mice. Further experiments confirmed that FTS·B inhibited the formation of NLRP3 inflammasome in microglia and astrocytes, thereby suppressing neuroinflammation and GSDMD-mediated pyroptosis. Altogether, these results suggest that FTS·B treatment attenuates central neuroinflammation and pyroptosis by inhibiting NLRP3 inflammasome of glial cells in EAE mice.

Femtoscopy correlation functions and mass distributions from production experiments

We discuss the relation between the Koonin-Pratt femtoscopic correlation function (CF) and invariant mass distributions from production experiments. We show that the equivalence is total for a zero source-size and that a Gaussian finite-size source provides a form-factor for the virtual production of the particles. Motivated by this remarkable relationship, we study an alternative method to the Koonin-Pratt formula, which connects the evaluation of the CF directly with the production mechanisms. The differences arise mostly from the T–matrix quadratic terms and increase with the source size. We study the case of the D0D*+ and D+D*0 correlation functions of interest to unravel the dynamics of the exotic Tcc(3875)+, and find that these differences become quite sizable already for 1 fm sources. We nevertheless conclude that the lack of coherence in high-multiplicity-event reactions and in the creation of the fire-ball source that emits the hadrons certainly make much more realistic the formalism based on the Koonin-Pratt equation. We finally derive an improved Lednicky-Lyuboshits (LL) approach, which implements a Lorentz ultraviolet regulator that corrects the pathological behavior of the LL CF in the punctual source-size limit. Published by the American Physical Society 2024

The C886T Mutation in the <i>TH</i> Gene Reduces the Activity of Tyrosine Hydroxylase in the Brain of Mice

Tyrosine hydroxylase (TH) catalyzes hydroxylation of L-tyrosine to L-3,4-dihydroxyphenylalanine, the initial and rate-limiting step in the synthesis of dopamine, noradrenaline, and adrenaline. Mutations in the human TH gene are associated with hereditary motor disorders. The common C886T mutation identified in the mouse Th gene results in the R278H substitution in the enzyme molecule. We investigated the impact of this mutation on the TH activity in the mouse midbrain. The TH activity in the midbrain of Mus musculus castaneus (CAST) mice homozygous for the 886C allele was higher compared to C57BL/6 and DBA/2 mice homozygous for the 886T allele. Notably, this difference in the enzyme activity was not associated with changes in the Th gene mRNA levels and TH protein content. Analysis of the TH activity in the midbrain in mice from the F2 population obtained by crossbreeding of C57BL/6 and CAST mice revealed that the 886C allele is associated with a high TH activity. Moreover, this allele showed complete dominance over the 886T allele. However, the C886T mutation did not affect the levels of TH protein in the midbrain. These findings demonstrate that the C886T mutation is a major genetic factor determining the activity of TH in the midbrain of common laboratory mouse strains. Moreover, it represents the first common spontaneous mutation in the mouse Th gene whose influence on the enzyme activity has been demonstrated. These results will help to understand the role of TH in the development of adaptive and pathological behavior, elucidate molecular mechanisms regulating the activity of TH, and explore pharmacological agents for modulating its function.

The Impact of Psychological Trauma on Deviant Behavior in Adolescents

This study examined psychological traumas that influence deviant behaviors in adolescents. Given adverse social, psychological, and familial conditions, adolescents predisposed to criminality often experience psychological disorders, familial dysfunction, and negative impacts from their social environment, all of which contribute to their deviant tendencies. The concepts of pathology and deviant behavior were introduced as the two central themes of this research. Additionally, the developmental stages of adolescents and the process of socialization are emphasized as foundational to identity formation and social adaptability. The primary research question was: What factors influence the emergence of deviant behaviors in adolescents? Evidence suggests that psychological and emotional disorders, unfavorable family conditions, and the influence of social and cultural environments increase the likelihood of deviant behavior. Utilizing an analytical-descriptive methodology, the study concludes that establishing a supportive and secure environment, particularly within the family and community, can contribute to the reduction of deviant behaviors. Consequently, the importance of collaboration among various institutions and a focus on educational strategies to foster positive identity development in adolescents and mitigate social deviance are highlighted.

Behavioral Test Scores Could Be Linked to the Protein Expression Values of p62 and GLAST in the Brains of Mice with Neuropsychiatric Disorder-Related Behaviors.

Neuropsychiatric disorders are a public health concern, in which diagnosis and prognosis may be based on clinical symptoms that might often diverge across individuals. Schizophrenia is a major neuropsychiatric disorder, which may affect millions worldwide. However, the biochemical alterations of this disorder have not been comprehensively distinguished. In addition, there is less confidence in finding specific biomarkers for neuropsychiatric disorders, including schizophrenia, but rather a specific characteristic behavioral pattern. In general, maternal immune activation is considered to be one of the important factors in the development of neuropsychiatric disorders. Here, a mouse model of neuropsychiatric disorders was created, in which poly I:C, sodium dextran sulfate (DSS), and κ-carrageenan (CGN) were utilized for maternal immune activation during the pregnancies of mother mice. Subsequently, we examined the link between biochemical changes in p62 and/or glutamate aspartate transporter (GLAST) in the brains of offspring mice and the alteration in their experimental behavior scores. Furthermore, a therapeutic study was conducted on these neuropsychiatric disorder model mice using butyric acid, piceid, and metformin. It was found that some molecules could effectively improve the behavioral scores of neuropsychiatric model mice. Importantly, significant correlations between certain behavioral scores and p62 protein expression, as well as between the scores and GLAST expression, were recognized. This is the first report of a significant correlation between pathological behaviors and biochemical alterations in neuropsychiatric disorder model animals. This concept could contribute to the development of innovative treatments to at least ameliorate the symptoms of several psychiatric disorders.

Evolving alterations of structural organization and functional connectivity in feedforward neural networks after induced P301L tau mutation.

Reciprocal structure-function relationships underlie both healthy and pathological behaviours in complex neural networks. Thus, understanding neuropathology and network dysfunction requires a thorough investigation of the complex interactions between structural and functional network reconfigurations in response to perturbation. Such adaptations are often difficult to study in vivo. For example, subtle, evolving changes in synaptic connectivity, transmission and the electrophysiological shift from healthy to pathological states, for example alterations that may be associated with evolving neurodegenerative disease, such as Alzheimer's, are difficult to study in the brain. Engineered in vitro neural networks are powerful models that enable selective targeting, manipulation and monitoring of dynamic neural network behaviour at the micro- and mesoscale in physiological and pathological conditions. In this study, we engineered feedforward cortical neural networks using two-nodal microfluidic devices with controllable connectivity interfaced with microelectrode arrays (mMEAs). We induced P301L mutated tau protein to the presynaptic node of these networks and monitored network dynamics over three weeks. Induced perturbation resulted in altered structural organization and extensive axonal retraction starting in the perturbed node. Perturbed networks also exhibited functional changes in intranodal activity, which manifested as an overall decline in both firing rate and bursting activity, with a progressive increase in synchrony over time and a decrease in internodal signal propagation between pre- and post-synaptic nodes. These results provide insights into dynamic structural and functional reconfigurations at the micro- and mesoscale as a result of evolving pathology and illustrate the utility of engineered networks as models of network function and dysfunction.

A Novel Compound Ligusticum Cycloprolactam Alleviates Neuroinflammation After Ischemic Stroke via the FPR1/NLRP3 Signaling Axis.

Microglia/macrophages, as pivotal immune cells in the central nervous system (CNS), play a critical role in neuroinflammation associated with ischemic brain injury. Targeting their activation through pharmacological interventions represents a promising strategy to alleviate neurological deficits, thereby harboring significant implications for the prevention and treatment of ischemic stroke. Ligusticum cycloprolactam (LIGc), a novel monomeric derivative of traditional Chinese medicine, has shown potential as a therapeutic agent; however, its specific role in cerebral ischemic injury remains unclear. In vitro experiments utilized lipopolysaccharide (LPS)-induced inflammation models of RAW264.7 cells and primary mouse microglia. Invivo studies employed LPS-induced neuroinflammation models in mice and a transient middle cerebral artery occlusion (tMCAO) mouse model to evaluate the impact of LIGc on neuroinflammation and microglia/macrophage phenotypic alterations. Further elucidation of the molecular mechanisms underlying these effects was achieved through RNA-Seq analyses. LIGc exhibited the capacity to attenuate LPS-induced production of pro-inflammatory markers in macrophages and microglia, facilitating their transition to an anti-inflammatory phenotype. In models of LPS-induced neuroinflammation and tMCAO, LIGc ameliorated pathological behaviors and neurological deficits while mitigating brain inflammation. RNA-seq analyses revealed formyl peptide receptor 1 (FPR1) as a critical mediator of LIGc's effects. Specifically, FPR1 enhances the pro-inflammatory phenotype of microglia/macrophages and inhibits their anti-inflammatory response by upregulating NLR family pyrin domain protein 3 (NLRP3) inflammasomes, thus aggravating inflammatory processes. Conversely, LIGc exerts anti-inflammatory effects by downregulating the FPR1/NLRP3 signaling axis. Furthermore, FPR1 overexpression or NLRP3 agonists reversed the effects of LIGc observed in this study. Our findings suggest that LIGc holds promise in improving ischemic brain injury and neuroinflammation through modulation of microglia/macrophage polarization. Mechanistically, LIGc attenuates the pro-inflammatory phenotype and promotes the anti-inflammatory phenotype by targeting the FPR1/NLRP3 signaling pathway, ultimately reducing inflammatory responses and mitigating neurological damage.

Circuit mechanisms underlying sexually dimorphic outcomes of early life stress.

Stress during early life influences brain development and can affect social, motor, and emotional processes. We describe a striking sex difference in the effects of early life stress (ELS), which produces anhedonia and anxiety-like behaviors in female adolescent mice, as reported previously, but repetitive behavioral pathology and social deficits in male adolescent mice. Notably, this parallels sex differences seen in the prevalence of psychiatric symptoms: depression and anxiety disorders are more common in girls and women, whereas neurodevelopmental disorders like autism spectrum disorder and Tourette syndrome are markedly more common in boys and men. We characterized the effects of ELS on the medial prefrontal cortex (mPFC) and on its projections to the dorsal striatum (dStr) and lateral septum (LS). ELS males, but not females, developed hyperactivity in the cortico-striatal circuit and hypoactivity in the cortico-septal circuit. Chemogenetic manipulation of cortico-striatal projection neurons modulates repetitive behavioral pathology and social behaviors in stressed males, and anhedonia in stressed females. Activation of cortico-septal projection neurons rescues social deficits in stressed males. We conclude that early life stress produces sexually dimorphic behavioral effects, with potential relevance to human psychiatric symptoms, through its differential effects on cortico-striatal and cortico-septal circuits.

A randomized, double-blind, placebo-controlled clinical trial to evaluate pregabalin efficacy in the treatment of behavioral and psychological symptoms of dementia in patients with Alzheimer's disease.

Behavioral and Psychological Symptoms of Dementia (BPSD) are common during Alzheimer's disease and cause severe problems for patients and their caregivers. To assess the therapeutic efficacy of Pregabalin in comparison with a placebo in treating BPSD in patients with Alzheimer's disease (AD) visiting the memory and cognition clinic of Roozbeh Psychiatric Hospital in Tehran, Iran. A 12-week double-blind, randomized comparison of Pregabalin and placebo treatments was conducted in 53 patients with DSM-V diagnosis of dementia of Alzheimer's type. They were randomly assigned to receive Pregabalin (doses: 50 titrated up to 300 mg/day) or a placebo. Clinical response was evaluated using the Neuropsychiatric Inventory (NPI), and the Behavioral Pathology in AD Rating Scale (BEHAVE-AD) scores compared with baseline. Side effects were also recorded carefully. Patients receiving Pregabalin had better outcomes in comparison with patients receiving a placebo regarding both NPI and BEHAVE-AD scores after 12 weeks (p-value = 0.009 for NPI and p-value = 0.003 for BEHAVE-AD). There was also a statistically significant decrease in the treatment group depression sub-score regarding NPI and BEHAVE-AD (respectively, p-value =0.000, 0.003). The caregiver burden sub-score of the NPI test was also lower in patients receiving pregabalin (p-value = 0.000). There was no statistically significant difference between the occurrence of adverse effects between the two groups (p-value = 1.00). Pregabalin at a dose of 300 mg/day was well tolerated and associated with reductions in the severity and frequency of behavioral symptoms in patients with AD. Pregabalin could be considered a favorable choice for treating BPSD in adults with mild to moderate stages of Alzheimer 's-type dementia, considering its befitting safety profile. https://www.irct.ir/trial/52750, identifier IRCT20201201049553N1.

The MRL Model: A Valuable Tool in Studies of Autoimmunity-Brain Interactions.

The link between systemic autoimmunity, brain pathology, and aberrant behavior is still largely unexplored field of biomedical science. Accumulating evidence points to causal relationships between immune factors, neurodegeneration, and neuropsychiatric manifestations. By documenting autoimmunity-associated neuronal degeneration and cytotoxicity of the cerebrospinal fluid from disease-affected subjects, the murine MRL model has shown high validity in revealing principal pathogenic circuits. In addition, unlike any other autoimmune strain, MRL mice produce antibodies commonly found in patients suffering from lupus and other autoimmune disorders. This review highlights the importance of the MRL model as a useful preparation for understanding the links between the immune system and brain function.

EPID-20. PRIMARY INTRAMEDULLARY PILOMYXOID ASTROCYTOMA OF SPINAL CORD (PIPASC): A SYSTEMATIC REVIEW OF CASE REPORTS AND CASE SERIES OF TWO DECADES

Abstract BACKGROUND Pilomyxoid Astrocytoma (PMA), new variant of pilocytic astrocytoma, is more aggressive and relatively rare, mostly seen in children and commonly found in brain. Primary intramedullary pilomyxoid astrocytoma of spinal cord (PIPASC) is extremely rare. The distinct aggressive and pathological behavior, poor prognosis and the diversity in response to various treatment modalities makes the PIPASC an oncologic enigma. We aim to evaluate the clinical manifestations, histopathologic spectrum and onco-surgical management of this neoplasm. MATERIALS AND METHODS After an extensive literature search using PubMed Central and Google Scholar, eight case reports and one case series of patients with spinal PA were retrieved and included using the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines without applying any filter of time, study type or place. Case presentations of 12 patients were analyzed in this review. RESULTS Pediatric preponderance of the neoplasm (75%) with the mean age of 7.90 ± 4.51 years was noted. Sensory deficits and scoliotic deformity were the most common presenting symptom and sign in 83.33% and 33.33% of patients, respectively. Thoracic spine (50%) was most commonly affected region. MRI showed the most consistent findings of cord compression in 100% cases and the lesion appeared hypointense on T1- weighted images (T1WI) and hyperintense on T2-weighted images (33.33%). The average post treatment survival duration was found to be more than 2 years. CONCLUSIONS Occurrence of PIPASC among pediatric population is rare. They have possibility of extraneural metastasis, can differentiate into more malignant glioma and get recurrent due to which they require a long-term follow-up of the patients. Further studies are required to investigate the utility of chemotherapy and radiotherapy in its management.

TRANCE STEREOTYPIES IN HUMAN AND PRIMATE PANTOMIMICRY

The authors reviewed and analysed Russian and foreign experimental studies on pantomimic stereotypes. Initially, stereotypical behaviuor was negatively evaluated. Modern research considers adaptive functions and possibilities of self-stimulation as a way to harmonise emotional and mental state. A comparative analysis of circular, pendulum and diagonal movements in children and Old World monkeys was conducted using an ethological approach to the study of behavioural patterns. Human observations were conducted in the psychoneurological department of Silischeva Astrakhan Regional Children’s Clinical Hospital, 40 preschool children with mental dysontogenesis participated. Five laboratory macaques and a family of hamadryas baboons kept in an aviary with homologous kinesics were observed in Sukhumi nursery. According to the authors’ team, walking (running) in a circle and diagonally, swinging the body “right-to-leftˮ in the pantomimic production of children and monkeys are associated with self-stimulation of an altered state of consciousness. Trance stereotypes divert attention from external stressors and stimuli and harmonise mental homeostasis. The study may be of interest to anthropologists, primatologists, specialists in the study of the psyche and pathological behaviour of animals and Homo sapiens.

A promising drug repurposing approach for Alzheimer's treatment: Givinostat improves cognitive behavior and pathological features in APP/PS1 mice

Alzheimer's disease (AD) is the most common neurodegenerative disease, characterized by memory loss, speech and motor defects, personality changes, and psychological disorders. The exact cause of AD remains unclear. Current treatments focus on maintaining neurotransmitter levels or targeting β-amyloid (Aβ) protein, but these only alleviate symptoms and do not reverse the disease. Developing new drugs is time-consuming, costly, and has a high failure rate. Utilizing multi-omics for drug repositioning has emerged as a new strategy. Based on transcriptomic perturbation data of over 40,000 drugs in human cells from the LINCS-L1000 database, our study employed the Jaccard index and hypergeometric distribution test for reverse transcriptional feature matching analysis, identifying Givinostat as a potential treatment for AD. Our research found that Givinostat improved cognitive behavior and brain pathology in models and enhanced hippocampal synaptic plasticity. Transcriptome sequencing revealed increased expression of mitochondrial respiratory chain complex proteins in the brains of APP/PS1 mice after Givinostat treatment. Functionally, Givinostat restored mitochondrial membrane potential, reduced reactive oxygen species, and increased ATP content in Aβ-induced HT22 cells. Additionally, it improved mitochondrial morphology and quantity in the hippocampus of APP/PS1 mice and enhanced brain glucose metabolic activity. These effects are linked to Givinostat promoting mitochondrial biogenesis and improving mitochondrial function. In summary, Givinostat offers a promising new strategy for AD treatment by targeting mitochondrial dysfunction.

Implementations of sign- and goal-tracking behavior in humans: A scoping review.

Animal research has identified two major phenotypes in the tendency to attribute incentive salience to a reward-associated cue. Individuals called "sign-trackers" (STs) preferentially approach the cue, assigning both predictive and incentive values to it. In contrast, individuals called "goal-trackers" (GTs) preferentially approach the location of the upcoming reward, assigning only a predictive value to the cue. The ST/GT model has been shown to be relevant to understanding addiction vulnerability and other pathological behaviors in animals. Therefore, recent studies tried to implement this animal model in the human population. This scoping review aimed to identify and map evidence of human sign- and goal-tracking. Studies that explicitly measured human sign- and goal-tracking or related phenomena (e.g., attentional bias induced by reward-related cues), using paradigms in line with the animal model, were eligible for this review. We searched for published, unpublished, and gray literature (PhD theses, posters, conference papers) through the following databases: MEDLINE, Scopus, PsycINFO, Embase, OSF, and Google Scholar. The JBI scoping review methodology was adopted. Screening and extraction were carried out by three reviewers, in pairs. A total of 48 studies were identified. These studies used various experimental paradigms and used the term "sign-tracking" inconsistently, sometimes implicitly or not at all. We conclude that the literature on human sign-tracking is very heterogeneous on many levels. Overall, evidence supports the existence of sign- and goal-tracking behaviors in humans, although further validated research is crucially needed.

Maternal exploitation: impact of maternal food snatching behaviour on the growth of their offspring in Japanese macaques.

There is little information on maternal behaviour that deprives offspring of food, but some Japanese macaque, Macaca fuscata, mothers have been observed to snatch food from their offspring and eat it. This study investigated maternal food snatching behaviour (MFSB) and its impact on the growth of their offspring in provisioned, free-ranging Japanese macaques. The amount of food a mother snatched from her offspring was estimated to be 51.2% by dry weight compared to the amount of solid food an infant of the same age took in. Body mass growth of affected infants indicated a below-average mass gain. The study suggests that MFSB might be a pathological behaviour and provides the first detailed account of parental exploitation in animals.

Body, image, and digital technology in adolescence and contemporary youth culture.

The physical, psychological and social changes that occur during adolescence constitute a physiological crisis that is necessary for development and growth. The establishment of a suitable "self-image" is important for facilitating harmonious psychophysical development during this time. In the current era, digital technology (DT) serves as an extraordinary means of communication for young people, who make significant use of images as a mode of expression. Accordingly, there is growing interest in the relationship between physical development, self-image and use of DT. A review of the published literature on the topic was carried out in April 2024. Fourteen studies (n = 14) were inclused from search of electronic databases such as PubMed, CINAHL, PsycInfo, MedLine, and Cochrane Library. The aim of this study is to explore the influence of (DT) on cultural models of adolescent body image, and how this "social" culture can affect wellbeing and development. It was considered that the rise of DT and social media (SM) emphasized in young people the culture of appearance, adherence to ideal models (thinness ideal) and social comparison at an unprecedented level. It was estimated that the digital mechanism works on the adolescent's vulnerability and stimulates the desire for experimentation and amplifies cultural beliefs that expose the young to deviant or pathological behaviors on the body. The use of digital images emphasizes the perception of self by making it more real and alive but empty of content. Our framework highlights that the adolescent can defend himself if he leaves the homologation that the SM condition, regains his own experiences, fill with emotional content and real life the images and the representation of the body.