The motivation to integrate and perceived discrimination as antecedents of cultural identity styles.

OBJECTIVES: The research examined the motivation to integrate and perceived discrimination as antecedents of cultural identity styles, the cognitive and behavioral strategies that bicultural individuals use for decision making in managing and maintaining their ethnic and national identities. Two major cultural identity styles have been distinguished: the alternating identity style (AIS, changing cultural identities depending on the circumstances) and the hybrid identity style (HIS, blending selected aspects of these identities in a unique way). Based on earlier cross-sectional research, we tested the hypotheses that the motivation to integrate would predict greater use of both styles and that perceived discrimination would predict greater use of the AIS, but not the HIS, over time. METHOD: A community sample of 493 Chinese Americans (56% female, 51.5% first generation, Mage = 53.27 years) completed an online survey at two points in time with approximately a 1-month interval. Path modeling controlling for demographic factors (age, generation) and cultural identity style (AIS and HIS at T1) was used to test our hypotheses. RESULTS: Analyses revealed that younger Chinese Americans made greater use of the AIS and that both the motivation to integrate and perceived discrimination were significant predictors of the AIS at T2. In contrast, only the motivation to integrate predicted the HIS at T2, confirming our hypotheses. CONCLUSIONS: The results demonstrate that both personal and situational factors affect the management of cultural identities. The findings are discussed in relation to research on acculturation and integration and theories of social and situated identity identities. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Exploring the place attachments of older migrants in Aotearoa: A life course history approach.

Migrants are faced with the task of creating a sense of home in a new context. As migrants grow older in their host countries, they are also making important decisions on where to live out the rest of their lives, making salient the places they attach themselves to. Place attachment, and its subcomponents of place identity and place dependence, are concepts that have been explored in the ageing and migration literature, demonstrating that positive, emotional attachments to places are positively correlated with better health outcomes. Although it has been established that individuals' attachments to places are dynamic, multidimensional and change over the life course, there is a paucity of research exploring the place attachments of migrants as they age using a life course approach. This study adopted a life course approach to investigate how the components of place attachment shifted over time for migrant people in Aotearoa New Zealand as they aged, and to better understand the mechanisms and barriers to establishing a sense of home in a foreign land. We examined the narratives of ten older migrants (65 years or older) who migrated to Aotearoa before the age of 50. Key findings illustrated that all participants had strong place identities (i.e., explicit self-identification and sense of belonging) to their countries of origin before migrating to Aotearoa, all participants developed strong place dependence (i.e., fulfilment of functional needs) to Aotearoa over their life course, but not everyone was able to develop place identity to Aotearoa. Mechanisms such as language, cultural attitudes, and values can both facilitate and prevent attachments to either home or host country. These results uncover how Aotearoa's ageing migrants negotiate their attachments to places over the life course.

Emerging Translational Research in Neurological and Psychiatric Diseases: From In Vitro to In Vivo Models.

Revealing the underlying pathomechanisms of neurological and psychiatric disorders, searching for new biomarkers, and developing novel therapeutics all require translational research [...].

Profiles of acculturative strategies and cultural stressors among Hispanic/Latinx college-attending emerging adults.

OBJECTIVE: The present study identified unique profiles of cultural stressors (i.e., bicultural stress, discrimination, and negative context of reception) and acculturative strategies (i.e., heritage practices, heritage identification, U.S. practices, and U.S. identification), in Hispanic/Latinx (HL) emerging adults. Additionally, we examined associations between positive and negative psychosocial functioning, with profiles of acculturative strategies and cultural stressors. METHOD: The present study utilized a baseline sample of 779 HL college students (75.8% female, Mage = 20.80 years, SD = 2.66) drawn from a daily diary study on acculturation. RESULTS: Latent profile analysis identified four distinct profiles. The Bicultural and Low Cultural Stressors (B-LowCS; 53.55%) was marked by strong heritage and U.S. cultural orientation and low levels across all cultural stressors. The Marginalization and High Acculturative Stressors (M-HighAS; 20.13%) was marked by weak heritage and U.S. cultural orientation, high acculturative stressors, and low discrimination. The third profile, the Heritage Rejection and Low Cultural Stressors (HR-LowCS; 16.05%) was marked by rejection of heritage culture and low cultural stressors. Finally, the Separation and High Cultural Stressors (S-HighCS; 10.26%) was marked by weak U.S. cultural orientation and high cultural stressors. Consistent with past research, the B-LowCS profile was marked by the highest level of positive psychosocial functioning and the lowest levels of internalizing and externalizing symptoms. CONCLUSIONS: The results of the present study highlight the usefulness of person-centered approaches for understanding the interplay between acculturative strategies and cultural stressors, and the implications of these distinct profiles on psychosocial functioning in HL emerging adults. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

From CGRP to PACAP, VIP, and Beyond: Unraveling the Next Chapters in Migraine Treatment.

Migraine is a neurovascular disorder that can be debilitating for individuals and society. Current research focuses on finding effective analgesics and management strategies for migraines by targeting specific receptors and neuropeptides. Nonetheless, newly approved calcitonin gene-related peptide (CGRP) monoclonal antibodies (mAbs) have a 50% responder rate ranging from 27 to 71.0%, whereas CGRP receptor inhibitors have a 50% responder rate ranging from 56 to 71%. To address the need for novel therapeutic targets, researchers are exploring the potential of another secretin family peptide, pituitary adenylate cyclase-activating polypeptide (PACAP), as a ground-breaking treatment avenue for migraine. Preclinical models have revealed how PACAP affects the trigeminal system, which is implicated in headache disorders. Clinical studies have demonstrated the significance of PACAP in migraine pathophysiology; however, a few clinical trials remain inconclusive: the pituitary adenylate cyclase-activating peptide 1 receptor mAb, AMG 301 showed no benefit for migraine prevention, while the PACAP ligand mAb, Lu AG09222 significantly reduced the number of monthly migraine days over placebo in a phase 2 clinical trial. Meanwhile, another secretin family peptide vasoactive intestinal peptide (VIP) is gaining interest as a potential new target. In light of recent advances in PACAP research, we emphasize the potential of PACAP as a promising target for migraine treatment, highlighting the significance of exploring PACAP as a member of the antimigraine armamentarium, especially for patients who do not respond to or contraindicated to anti-CGRP therapies. By updating our knowledge of PACAP and its unique contribution to migraine pathophysiology, we can pave the way for reinforcing PACAP and other secretin peptides, including VIP, as a novel treatment option for migraines.

Thermal neuromodulation using pulsed and continuous infrared illumination in a penicillin-induced acute epilepsy model.

Infrared neuromodulation (INM) is a promising neuromodulation tool that utilizes pulsed or continuous-wave near-infrared (NIR) laser light to produce an elevation of the background temperature of the neural tissue. The INM-based cortical heating has been proven as an effective modality to induce changes in neuronal activities. In this paper, we investigate the effect of INM-based cortical heating on the characteristics of interictal epileptiform discharges (IEDs) induced by penicillin in anesthetized rats. Cortical heating was conducted using a NIR laser light guided through a needle-like silicon-based waveguide probe. We detected penicillin-induced cortical IEDs from preprocessed micro-electrocorticography ([Formula: see text]ECoG) recordings, then we assessed changes in various temporal and spectral features of IEDs due to INM. Our findings show that the fast cortical heating phase obtained with continuous-wave NIR light is highly associated with a reduction of IED amplitudes, small but significant changes in the negative amplitude of IEDs compared with the baseline, and a proportional increase in the power of frequency bands related to delta/theta (2-8 Hz) and gamma (28-80 Hz) oscillations. Furthermore, a low rate of cortical heating with pulsed NIR illumination has a more inhibitory impact on the sharp negative polarity of IEDs. Our findings do not indicate a clear reduction in the frequency of IEDs in anesthetized rodents. In contrast, 2-4 min of continuous laser illumination leads to a notable increase in IED frequency. This effect of INM could potentially restrict its use in therapeutic applications related to epilepsy. However, the thermal effect of INM on cortical neurons induces changes in other characteristics of IEDs, which could prove beneficial for future applications.

Preclinical modeling in depression and anxiety: Current challenges and future research directions.

This editorial highlights the limitations of preclinical models in accurately reflecting the complexity of anxiety and depression, which leads to a lack of effective treatments for these disorders. Inconsistencies in experimental designs and methodologies can entail conflicting or inconclusive findings, while an overreliance on medication can mask underlying problems. Researchers are exploring new approaches to preclinical modeling of negative emotional disorders, including using patient-derived cells, developing more complex animal models, and integrating genetic and environmental factors. Advanced technologies, such as optogenetics, chemogenetics and neuroimaging, are also being employed to improve the specificity and selectivity of preclinical models. Collaboration and innovation across different disciplines and sectors are needed to address complex societal challenges, which requires new models of funding and support that prioritize cooperation and multidisciplinary research. By harnessing the power of technology and new ways of working, researchers can collaborate more effectively to bring about transformative change.

The Tryptophan-Kynurenine Metabolic System Is Suppressed in Cuprizone-Induced Model of Demyelination Simulating Progressive Multiple Sclerosis.

Progressive multiple sclerosis (MS) is a chronic disease with a unique pattern, which is histologically classified into the subpial type 3 lesions in the autopsy. The lesion is also homologous to that of cuprizone (CPZ) toxin-induced animal models of demyelination. Aberration of the tryptophan (TRP)-kynurenine (KYN) metabolic system has been observed in patients with MS; nevertheless, the KYN metabolite profile of progressive MS remains inconclusive. In this study, C57Bl/6J male mice were treated with 0.2% CPZ toxin for 5 weeks and then underwent 4 weeks of recovery. We measured the levels of serotonin, TRP, and KYN metabolites in the plasma and the brain samples of mice at weeks 1, 3, and 5 of demyelination, and at weeks 7 and 9 of remyelination periods by ultra-high-performance liquid chromatography with tandem mass spectrometry (UHPLC-MS/MS) after body weight measurement and immunohistochemical analysis to confirm the development of demyelination. The UHPLC-MS/MS measurements demonstrated a significant reduction of kynurenic acid, 3-hydoxykynurenine (3-HK), and xanthurenic acid in the plasma and a significant reduction of 3-HK, and anthranilic acid in the brain samples at week 5. Here, we show the profile of KYN metabolites in the CPZ-induced mouse model of demyelination. Thus, the KYN metabolite profile potentially serves as a biomarker of progressive MS and thus opens a new path toward planning personalized treatment, which is frequently obscured with immunologic components in MS deterioration.

Exploring Novel Therapeutic Targets in the Common Pathogenic Factors in Migraine and Neuropathic Pain.

Migraine and neuropathic pain (NP) are both painful, disabling, chronic conditions which exhibit some symptom similarities and are thus considered to share a common etiology. The calcitonin gene-related peptide (CGRP) has gained credit as a target for migraine management; nevertheless, the efficacy and the applicability of CGRP modifiers warrant the search for more effective therapeutic targets for pain management. This scoping review focuses on human studies of common pathogenic factors in migraine and NP, with reference to available preclinical evidence to explore potential novel therapeutic targets. CGRP inhibitors and monoclonal antibodies alleviate inflammation in the meninges; targeting transient receptor potential (TRP) ion channels may help prevent the release of nociceptive substances, and modifying the endocannabinoid system may open a path toward discovery of novel analgesics. There may exist a potential target in the tryptophan-kynurenine (KYN) metabolic system, which is closely linked to glutamate-induced hyperexcitability; alleviating neuroinflammation may complement a pain-relieving armamentarium, and modifying microglial excitation, which is observed in both conditions, may be a possible approach. Those are several potential analgesic targets which deserve to be explored in search of novel analgesics; however, much evidence remains missing. This review highlights the need for more studies on CGRP modifiers for subtypes, the discovery of TRP and endocannabinoid modulators, knowledge of the status of KYN metabolites, the consensus on cytokines and sampling, and biomarkers for microglial function, in search of innovative pain management methods for migraine and NP.

Integrating Armchair, Bench, and Bedside Research for Behavioral Neurology and Neuropsychiatry: Editorial.

"To learning much inclined, who went to see the Elephant (though all of them were blind) that each by observation might satisfy the mind" [...].

Principles of Resonance Energy Transfer.

This unit describes the basic principles of Förster resonance energy transfer (FRET). Beginning with a brief summary of the history of FRET applications, the theory of FRET is introduced in detail using figures to explain all the important parameters of the FRET process. After listing various approaches for measuring FRET efficiency, several pieces of advice are given on choosing the appropriate instrumentation. The unit concludes with a discussion of the limitations of FRET measurements followed by a few examples of the latest FRET applications, including new developments such as spectral flow cytometric FRET, single-molecule FRET, and combinations of FRET with super-resolution or lifetime imaging microscopy and with molecular dynamics simulations. © 2022 The Authors. Current Protocols published by Wiley Periodicals LLC.

Mitochondrial Impairment: A Common Motif in Neuropsychiatric Presentation? The Link to the Tryptophan-Kynurenine Metabolic System.

Nearly half a century has passed since the discovery of cytoplasmic inheritance of human chloramphenicol resistance. The inheritance was then revealed to take place maternally by mitochondrial DNA (mtDNA). Later, a number of mutations in mtDNA were identified as a cause of severe inheritable metabolic diseases with neurological manifestation, and the impairment of mitochondrial functions has been probed in the pathogenesis of a wide range of illnesses including neurodegenerative diseases. Recently, a growing number of preclinical studies have revealed that animal behaviors are influenced by the impairment of mitochondrial functions and possibly by the loss of mitochondrial stress resilience. Indeed, as high as 54% of patients with one of the most common primary mitochondrial diseases, mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes (MELAS) syndrome, present psychiatric symptoms including cognitive impairment, mood disorder, anxiety, and psychosis. Mitochondria are multifunctional organelles which produce cellular energy and play a major role in other cellular functions including homeostasis, cellular signaling, and gene expression, among others. Mitochondrial functions are observed to be compromised and to become less resilient under continuous stress. Meanwhile, stress and inflammation have been linked to the activation of the tryptophan (Trp)-kynurenine (KYN) metabolic system, which observably contributes to the development of pathological conditions including neurological and psychiatric disorders. This review discusses the functions of mitochondria and the Trp-KYN system, the interaction of the Trp-KYN system with mitochondria, and the current understanding of the involvement of mitochondria and the Trp-KYN system in preclinical and clinical studies of major neurological and psychiatric diseases.

Modelling the neurodevelopmental pathogenesis in neuropsychiatric disorders. Bioactive kynurenines and their analogues as neuroprotective agents-in celebration of 80th birthday of Professor Peter Riederer.

Following introduction of the monoamine oxidase type B inhibitor selegiline for the treatment of Parkinson's disease (PD), discovery of the action mechanism of Alzheimer's disease-modifying agent memantine, the role of iron in PD, and the loss of electron transport chain complex I in PD, and development of the concept of clinical neuroprotection, Peter Riederer launched one of the most challenging research project neurodevelopmental aspects of neuropsychiatric disorders. The neurodevelopmental theory holds that a disruption of normal brain development in utero or during early life underlies the subsequent emergence of neuropsychiatric symptoms during later life. Indeed, the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition and the International Classification of Diseases, 11th Revision categorize autism spectrum disorder and attention deficit hyperactivity disorder in neurodevelopmental disorders (NDDs). More and more evidence, especially from preclinical studies, is revealing that neurodevelopmental pathology is not limited to the diagnostic class above, but also contributes to the development of other psychiatric disorders such as schizophrenia, bipolar disorder, and obsessive-compulsive disorder as well as neurodegenerative diseases such as PD and Huntington's disease. Preclinical animal research is taking a lead in understanding the pathomechanisms of NDDs, searching for novel targets, and developing new neuroprotective agents against NDDs. This narrative review discusses emerging evidence of the neurodevelopmental etiology of neuropsychiatric disorders, recent advances in modelling neurodevelopmental pathogenesis, potential strategies of clinical neuroprotection using novel kynurenine metabolites and analogues, and future research direction for NDDs.

Development and Validation of a Short Form Version of the Ethno-Cultural Identity Conflict Scale (EICS-SF).

A short form version of the Ethno-Cultural Identity Conflict Scale (ECIS-SF) was developed and validated to address item redundancy in the original scale and to increase its utility in comparative studies and applied settings. Construct, discriminant, nomological, and predictive validity of the EICS-SF was tested and supported with five samples in three countries. In Study 1, the EICS-SF was derived and validated using data from Chinese (n = 232) and Greek (n = 139) New Zealanders. Study 2 confirmed the factor structure, measurement equivalence and discriminant validity of the EICS-SF with Chinese Canadians (n = 199) and British Indians (n = 190). Study 3 provided additional evidence for the test-retest reliability and temporal consistency of the EICS-SF's association with criterion measures in Indian New Zealanders (n = 147). The EICS-SF is psychometrically sound and easy to administer with diverse populations. Potential for application in clinical settings is discussed.

Co-Players in Chronic Pain: Neuroinflammation and the Tryptophan-Kynurenine Metabolic Pathway.

Chronic pain is an unpleasant sensory and emotional experience that persists or recurs more than three months and may extend beyond the expected time of healing. Recently, nociplastic pain has been introduced as a descriptor of the mechanism of pain, which is due to the disturbance of neural processing without actual or potential tissue damage, appearing to replace a concept of psychogenic pain. An interdisciplinary task force of the International Association for the Study of Pain (IASP) compiled a systematic classification of clinical conditions associated with chronic pain, which was published in 2018 and will officially come into effect in 2022 in the 11th revision of the International Statistical Classification of Diseases and Related Health Problems (ICD-11) by the World Health Organization. ICD-11 offers the option for recording the presence of psychological or social factors in chronic pain; however, cognitive, emotional, and social dimensions in the pathogenesis of chronic pain are missing. Earlier pain disorder was defined as a condition with chronic pain associated with psychological factors, but it was replaced with somatic symptom disorder with predominant pain in the Diagnostic and Statistical Manual of Mental Disorders, 5th Edition (DSM-5) in 2013. Recently clinical nosology is trending toward highlighting neurological pathology of chronic pain, discounting psychological or social factors in the pathogenesis of pain. This review article discusses components of the pain pathway, the component-based mechanisms of pain, central and peripheral sensitization, roles of chronic inflammation, and the involvement of tryptophan-kynurenine pathway metabolites, exploring the participation of psychosocial and behavioral factors in central sensitization of diseases progressing into the development of chronic pain, comorbid diseases that commonly present a symptom of chronic pain, and psychiatric disorders that manifest chronic pain without obvious actual or potential tissue damage.

Immune Influencers in Action: Metabolites and Enzymes of the Tryptophan-Kynurenine Metabolic Pathway.

The tryptophan (TRP)-kynurenine (KYN) metabolic pathway is a main player of TRP metabolism through which more than 95% of TRP is catabolized. The pathway is activated by acute and chronic immune responses leading to a wide range of illnesses including cancer, immune diseases, neurodegenerative diseases and psychiatric disorders. The presence of positive feedback loops facilitates amplifying the immune responses vice versa. The TRP-KYN pathway synthesizes multifarious metabolites including oxidants, antioxidants, neurotoxins, neuroprotectants and immunomodulators. The immunomodulators are known to facilitate the immune system towards a tolerogenic state, resulting in chronic low-grade inflammation (LGI) that is commonly present in obesity, poor nutrition, exposer to chemicals or allergens, prodromal stage of various illnesses and chronic diseases. KYN, kynurenic acid, xanthurenic acid and cinnabarinic acid are aryl hydrocarbon receptor ligands that serve as immunomodulators. Furthermore, TRP-KYN pathway enzymes are known to be activated by the stress hormone cortisol and inflammatory cytokines, and genotypic variants were observed to contribute to inflammation and thus various diseases. The tryptophan 2,3-dioxygenase, the indoleamine 2,3-dioxygenases and the kynurenine-3-monooxygenase are main enzymes in the pathway. This review article discusses the TRP-KYN pathway with special emphasis on its interaction with the immune system and the tolerogenic shift towards chronic LGI and overviews the major symptoms, pro- and anti-inflammatory cytokines and toxic and protective KYNs to explore the linkage between chronic LGI, KYNs, and major psychiatric disorders, including depressive disorder, bipolar disorder, substance use disorder, post-traumatic stress disorder, schizophrenia and autism spectrum disorder.

Alcohol use trajectories across the life course: Influences of childhood predictors and consequences for late-life health.

BACKGROUND: The cumulative, negative health effects of alcohol consumption are exacerbated in older adulthood. We used a 'life course epidemiology' approach to explore how alcohol use trajectories develop across the lifespan, what early life events influence these trajectories and their associations with late-life health. METHODS: Survey data combined with retrospective life course history interviews were collected from 749 non-lifetime alcohol abstainer adults aged 61-81 years (51 % female). Frequency and quantity items of the AUDIT-C assessed alcohol use across each decade of life. Early life factors were childhood socioeconomic status, parental health behaviours, and age of drinking onset. Health outcomes were alcohol-related conditions. RESULTS: Latent class growth analysis yielded two life course trajectories for women: consistently infrequent, low quantity drinking (Group 1: 48 %) and increasingly frequent, low quantity drinking (Group 2: 52 %). Men showed three trajectories: consistently infrequent, low quantity drinking (Group 3: 36 %); increasingly frequent, low quantity drinking (Group 4: 51 %); and drinking with increasing frequency and quantity until midlife, after which consumption gradually declined (Group 5: 13 %). Better childhood socioeconomic status was associated with Groups 2 and 4. Later drinking onset was associated with Groups 1 and 3. Parental alcohol misuse, early drinking initiation and childhood socioeconomic adversity were predictive of Group 5. Those in Group 5 were five-to-seven times more likely to have alcohol-related comorbidities. CONCLUSIONS: Early life experiences influence life course hazardous alcohol use. Interventions across the life course, from childhood, when drinking may be initiated, through to older adulthood, when sensitivity to alcohol increases, are needed.

One slope does not fit all: longitudinal trajectories of quality of life in older adulthood.

PURPOSE: Maintaining or improving quality of life (QoL) in later life has become a major policy objective. Yet we currently know little about how QoL develops at older ages. The few studies that have modelled QoL change across time for older adults have used 'averaged' trajectories. However, this ignores the variations in the way QoL develops between groups of older adults. METHODS: We took a theoretically informed 'capabilities approach' to measuring QoL. We used four waves of data, covering 6 years, from the New Zealand Health, Work and Retirement Study (NZHWR) (N = 3223) to explore whether distinct QoL trajectories existed. NZHWR is a nationally representative longitudinal study of community-dwelling adults aged 50 + in New Zealand. Growth mixture modelling was applied to identify trajectories over time and multinomial regressions were calculated to test baseline differences in demographic variables (including age, gender, ethnicity, education and economic living standards). RESULTS: We found five QoL trajectories: (1) high and stable (51.94%); (2) average and declining (22.74%); (3) low and increasing (9.62%); (4) low and declining (10.61%); (5) low and stable (5.09%). Several differences across profiles in baseline demographic factors were identified, with economic living standards differentiating between all profiles. CONCLUSIONS: The trajectory profiles demonstrate that both maintaining and even improving QoL in later life is possible. This has implications for our capacity to develop nuanced policies for diverse groups of older adults.