Biomarkers in Neuropsychiatry最新文献

{"title":"Anxiety, stress, and the moderating role of ethnicity: Extending Tannous Haddad et al. (2026) beyond the Israeli context","authors":"Retche Poquita Colegado,&nbsp;Xyle Fe Adiong Verbal,&nbsp;Mariza Pechora Manlagaylay","doi":"10.1016/j.bionps.2026.100137","DOIUrl":"10.1016/j.bionps.2026.100137","url":null,"abstract":"<div><div>Does resilience protect everyone equally? Tannous Haddad, Barel, and Tzischinsky (2026) answer with a striking finding: resilience buffers anxiety only among Arab citizens of Israel, not among Jewish participants. This discovery dismantles universal assumptions about resilience and demands a culturally grounded rethinking. We extend this pivotal insight to the Philippines, where Muslim Filipino and Indigenous Lumad communities endure a conflict landscape defined not only by violence but also by deep seated historical injustice, marginalization, and fractured state relations. Anchored in the socioecological model of resilience (Ungar, 2011), we argue that the original study’s distinction between anxiety as a “temporally diffused emotional state” and stress as an acute emergency response (Daviu et al., 2019) holds the key to understanding differential distress across ethnic lines. For marginalized minorities, anxiety is chronic, shaped by generations of exclusion and uncertainty. For majority populations, stress is acute, triggered by immediate threat. This distinction reframes war related mental health: interventions that treat anxiety as a universal condition risk failure where structural vulnerability goes unaddressed. We translate these findings into actionable policy grounded in the <span><span>Philippine Mental Health Act (Republic Act No. 11036, 2018)</span></span>, calling for culturally congruent assessment, community embedded interventions codesigned with Imams, Datus, and traditional healers, and investment in local culture brokers who bridge trust gaps between communities and formal mental health systems. Resilience is not a trait to be built. It is a resource that communities already possess, waiting to be recognized and supported on their own cultural terms.</div></div>","PeriodicalId":52767,"journal":{"name":"Biomarkers in Neuropsychiatry","volume":"14 ","pages":"Article 100137"},"PeriodicalIF":0.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148193675","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Associations of social and genetic background variables to neuro-cognitive biomarkers of psychosis","authors":"Parker V. Jarrett ,&nbsp;Kiernan L. O’Mara ,&nbsp;Audrey L. Berardi ,&nbsp;Kelsey E. Roberts ,&nbsp;John T. Greco ,&nbsp;Rebekah L. Trotti ,&nbsp;David A. Parker ,&nbsp;Sarah K. Keedy ,&nbsp;Godfrey D. Pearlson ,&nbsp;Matcheri S. Keshavan ,&nbsp;S. Kristian Hill ,&nbsp;Elena I. Ivleva ,&nbsp;Carol A. Tamminga ,&nbsp;Jennifer E. McDowell ,&nbsp;Ezra Susser ,&nbsp;Brett A. Clementz","doi":"10.1016/j.bionps.2025.100134","DOIUrl":"10.1016/j.bionps.2025.100134","url":null,"abstract":"<div><div>Socioeconomic (SES) and ethno-racial factors may tilt psychosis diagnoses for persons from different backgrounds. Clinical diagnoses depend on patient and informant reports and are suspected of being susceptible to unintended bias. Diagnoses using laboratory tests are thought to be objective. Social disadvantages, however, alter brain functions related to psychosis. Race and class bias in laboratory medical diagnostics is an area of concern. To probe these issues for psychosis diagnoses, we describe relationships of SES, race/ethnicity, and ancestral genetic background to 11 integrated laboratory bio-factors that are associated with DSM categories and distinguish B-SNIP Biotypes. A series of analyses evaluated relationships of social factors and ancestry-related genetic background to those bio-factors: (i) canonical correlation revealed that SES and race (a social construct) are strongly associated (r²=.305) with cognitive performance and measures of brain physiology (prominently ERP magnitudes); genetic background neither significantly added to nor altered the structure of those associations; (ii) regression models illustrated that cognitive performance, intrinsic brain activity, and ERP magnitudes are substantially to modestly predicted by SES/race/genetic background, with SES/race accounting for the most variance on cognitive performance (approximately 25 %); (iii) regardless of including SES/race in differential diagnosis models, group differences between psychosis Biotypes were largely (85 %) preserved on bio-factor scores. For DSM diagnoses, less than 11 % of psychosis group differences were preserved. These outcomes illustrate that social factors are associated with psychosis-related laboratory tests. Nevertheless, SES/race did not substantially modify differential diagnosis of psychosis Biotypes. Using laboratory tests for psychosis differential diagnosis may facilitate the usefulness of stratification approaches, aid investigations of psychosis neurobiology and environmental risk, and improve treatment selections and approaches for all persons suffering with idiopathic psychosis.</div></div>","PeriodicalId":52767,"journal":{"name":"Biomarkers in Neuropsychiatry","volume":"13 ","pages":"Article 100134"},"PeriodicalIF":0.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145219171","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fatty acids as potential biomarkers of stearoyl-CoA desaturase inhibition: Variation in healthy subjects and Parkinson's disease patients","authors":"Pepijn P.N.M. Eijsvogel ,&nbsp;Andriy A. Gorbenko ,&nbsp;Dan F. Tardiff ,&nbsp;Michelle Skupien ,&nbsp;Ken Rhodes ,&nbsp;Robert H. Scannevin ,&nbsp;Yalcin Yavuz ,&nbsp;Emilie M.J. van Brummelen ,&nbsp;Brigitte Robertson ,&nbsp;Philip H.C. Kremer ,&nbsp;Geert Jan Groeneveld","doi":"10.1016/j.bionps.2025.100132","DOIUrl":"10.1016/j.bionps.2025.100132","url":null,"abstract":"<div><div>This study aimed to assess the naturally occurring variation in plasma fatty acids in healthy subjects and Parkinson’s disease (PD) patients. Alpha-synuclein (aSyn) plays a major role in Parkinson’s disease. Inhibition of stearoyl-CoA desaturase (SCD) reduces levels of mono-unsaturated C16 and C18 fatty acids, which are involved in aSyn toxicity in vitro and in vivo. The ratio of mono-unsaturated to saturated fatty acids (fatty acid desaturase index (FA-DI)) in plasma after SCD-inhibition correlates with effects on brain FA-DI. However, the FA-DI normal values and the inter- and intra-day variation in PD-patients and healthy subjects is unknown. Ten PD-patients (54 –73 years) and ten age-matched healthy subjects were included. On three consecutive days, fatty acids fractions and concentrations were measured throughout the day. Outcomes are expressed as estimated mean, and the coefficient of variation (CV%) in percentage. For C16 FA-DI, the inter-subject CV% was 20.7 % in healthy subjects, and 37.7 % in PD-patients. The intra-subject CV% over days was 14.0 % in healthy subjects, and 14.2 % in PD-patients, and within days 5.1 % in healthy subjects, and 5.9 % in PD-patients. For C18 FA-DI, the inter-subject CV% was 14.8 % in healthy subjects, and 16.0 % in PD-patients. The intra-subject CV% over days was 11.0 % in healthy subjects, and 8.6 % in PD-patients, and within days 8.4 % in healthy subjects, and 6.7 % in PD-patients. The observed extent of variability in healthy subjects and PD-patients support C16 and C18 FA-DI as suitable biomarkers to demonstrate target engagement in plasma, of for example SCD-inhibitors, in both healthy subjects and PD-patients.</div></div>","PeriodicalId":52767,"journal":{"name":"Biomarkers in Neuropsychiatry","volume":"13 ","pages":"Article 100132"},"PeriodicalIF":0.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144470218","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hippocampal glutamate and verbal episodic memory in the psychosis spectrum: A preliminary report","authors":"Nicolas R. Bolo ,&nbsp;Victor Zeng ,&nbsp;David Parker ,&nbsp;Elena Ivleva ,&nbsp;Jennifer McDowell ,&nbsp;Sarah Keedy ,&nbsp;Carol A. Tamminga ,&nbsp;Godfrey Pearlson ,&nbsp;Elliot S. Gershon ,&nbsp;Scott Hill ,&nbsp;Brett Clementz ,&nbsp;Matcheri Keshavan","doi":"10.1016/j.bionps.2025.100135","DOIUrl":"10.1016/j.bionps.2025.100135","url":null,"abstract":"<div><div>The Bipolar-Schizophrenia Network on Intermediate Phenotypes (B-SNIP) consortium categorized individuals with psychosis into 3 biologically distinct Biotypes (B1, B2, B3) based on cognitive and EEG measures. Deficient verbal episodic memory (VEM, a contributor to Biotype determination), is strongly associated with poor clinical outcome. Hippocampal glutamatergic circuits support VEM. Furthermore, glutamatergic mechanisms, implicated in cognitive and psychotic symptoms, are proposed as novel treatment targets. We used MRS to measure hippocampus glutamate and N-acetyl-aspartate (NAA) concentrations (non-contributors to Biotype) in psychosis vs. healthy-controls (HC). We examined VEM vs. glutamate relationships across DSM-IV diagnoses and Biotypes. We compared fits of linear and quadratic regression models. Glutamate was non-significantly lower in B1, higher in B2, and similar in B3 vs. HC. NAA did not differ. Quadratic models with Biotype-based groups provided best fits using the adjusted R² and AIC criteria. In B1, reduced glutamate tended to associate with deficient VEM, suggesting reduced excitatory glutamatergic signaling, which could be compensated by glutamate enhancing treatments, increasing production of synaptic glutamate or NMDAR mediated currents. In B2, higher glutamate and the accentuated inverted-U shaped VEM vs. glutamate relationship suggest high levels of dysregulated glutamatergic activity possibly related to deficient inhibitory GABAergic control. In B3, the independence of VEM and glutamate suggests that, in contrast to B1 and B2, B3 may be more sensitive to non-glutamatergic or GABAergic neurotransmitter system-targeted compounds to maintain healthy memory function. Because of the limited sample size, the interpretation of results is of a tentative nature. Results help explain the role of hippocampal glutamatergic neurotransmission in VEM deficits in psychotic disorders and motivate distinct treatment strategies for individuals with psychosis stratified by Biotype.</div></div>","PeriodicalId":52767,"journal":{"name":"Biomarkers in Neuropsychiatry","volume":"13 ","pages":"Article 100135"},"PeriodicalIF":0.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145683654","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Erratum to “Can neurocognitive assessment be a lower-cost substitute for biomarkers in predicting progression from mild cognitive impairment (MCI) to Alzheimer’s disease (AD)? A narrative review” Biomarkers in Neuropsychiatry, Volume 9 (2023), 100069","authors":"Lea Daou ,&nbsp;Alaeddine El Alayli ,&nbsp;Fadi Constantinos ,&nbsp;Georgette Dib ,&nbsp;Marc Barakat","doi":"10.1016/j.bionps.2025.100131","DOIUrl":"10.1016/j.bionps.2025.100131","url":null,"abstract":"","PeriodicalId":52767,"journal":{"name":"Biomarkers in Neuropsychiatry","volume":"13 ","pages":"Article 100131"},"PeriodicalIF":0.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145736696","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Is low-grade inflammation related to cognitive performance during a sustained attention task in depression? – A case-control study","authors":"Bruno Pedraz-Petrozzi ,&nbsp;Eva Kathrin Lamadé ,&nbsp;Nils Mischa Hübner ,&nbsp;Jil Zippelius ,&nbsp;Elena Neumann ,&nbsp;Gebhard Sammer","doi":"10.1016/j.bionps.2025.100121","DOIUrl":"10.1016/j.bionps.2025.100121","url":null,"abstract":"<div><div>This study aimed to investigate the associations between inflammatory cytokines and cognitive performance in individuals with depression compared to healthy controls, while accounting for variables, such as perceived fatigue, BMI, and age. Individuals diagnosed with depression (n = 23) and healthy controls (n = 31) were included in the study. A 15-minute sustained attention task (subtest of the Test Battery for Attention, version 2.3.1) was administered with concurrent electroencephalographic recordings to evaluate P300 amplitude and latency. Peripheral inflammation was assessed by measuring IL-6, IL-1β, and TNF-α levels. Perceived fatigue was assessed using the German version of the Fatigue Impact Scale. Generalized linear models (GLM) were used to evaluate the main aims of the study. Results indicated that depression was associated with reduced P300 amplitudes (p = 0.011), and age was significantly associated with P300 amplitude, with older participants showing reductions (p = 0.016). However, no significant effects of inflammatory markers on P300 components were found. While no group differences were observed in the total number of hits, both perceived fatigue (p = 0.033) and TNF-α (p = 0.007) were significantly associated with hit accuracy. A post-hoc mediation analysis explored that perceived fatigue mediates the relationship between depression and number of hits. These findings suggest that low-grade inflammation may not directly influence P300 components, though inflammation and fatigue appear linked to accuracy deficits. Finally, the impact of depression on the number of hits is primarily mediated by perceived fatigue, suggesting that fatigue is a crucial factor in how depression affects cognition.</div></div>","PeriodicalId":52767,"journal":{"name":"Biomarkers in Neuropsychiatry","volume":"12 ","pages":"Article 100121"},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143387470","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genetic predictors of attempted suicide among South Indian adolescents and young adults: A case-control study","authors":"Anju Mathew ,&nbsp;Ann Mary Alex ,&nbsp;Chathathayil Mohammedali Shafeeque ,&nbsp;Saboora Beegum Muthubeevi ,&nbsp;Vijayakumar Krishnapillai ,&nbsp;Moinak Banerjee","doi":"10.1016/j.bionps.2025.100126","DOIUrl":"10.1016/j.bionps.2025.100126","url":null,"abstract":"<div><h3>Background</h3><div>Suicide among adolescents and young adults is an alarming public health issue globally. Though studies suggest the link between genetic factors and suicidal behavior, there is a paucity of studies of specific genetic variants in adolescents and young adults. Hence this study explored the genetic predictors for attempted suicide among adolescents and young adults, by studying the genetic basis of serotonin and dopamine synthesis, transport, and degradation machinery.</div></div><div><h3>Methods</h3><div>A Case-control association study was conducted comprising individuals with attempted suicide (cases n = 80), 13–29 years of age, belonging to Malayalam speaking Dravidian population, and attending a tertiary care center in South India. Age, sex, and ethnicity matched controls (n = 267) with no history of attempted suicide were also considered from the same ethnic population. Genotyping was performed for functionally critical SNP in serotonin receptor, Tryptophan hydroxylase, Tyrosine hydroxylase, and Catechol-o-methyl transferase. Statistical significance for allelic and genotypic comparisons and their odds ratios were computed.</div></div><div><h3>Results</h3><div>The Tyrosine Hydroxylase THrs2070762 and Tryptophan Hydroxylase TPH1rs211105 genetic variants showed a statistically significant association with attempted suicide phenotype.</div></div><div><h3>Conclusion</h3><div>The study suggests that the genetic variants in Tyrosine Hydroxylase and Tryptophan Hydroxylase are predictive of attempted suicide among adolescents and young adults. Understanding the genetic variations will help in identifying and managing high-risk individuals.</div></div>","PeriodicalId":52767,"journal":{"name":"Biomarkers in Neuropsychiatry","volume":"12 ","pages":"Article 100126"},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143738876","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A systematic review of in vivo brain insulin resistance biomarkers in humans","authors":"Graham Reid ,&nbsp;Brendan Sargent ,&nbsp;Sarah Bauermeister ,&nbsp;Amanda Adler ,&nbsp;Ivan Koychev","doi":"10.1016/j.bionps.2025.100125","DOIUrl":"10.1016/j.bionps.2025.100125","url":null,"abstract":"<div><div>Type 2 diabetes mellitus (T2DM) is associated with an elevated risk of dementia, prompting interest into the concept of brain-specific insulin resistance. However, the brain's reliance on insulin-independent glucose transporters complicates attempts to measure in vivo brain insulin resistance using the definition of system-wide insulin resistance, which is based on glucose-insulin interactions. In this review, we explore three available biomarkers for evaluating in vivo brain-specific insulin resistance in humans: (1) correlating systemic insulin resistance with brain function, (2) examining functional brain changes after the administration of intranasal insulin, and (3) quantifying insulin signalling proteins in neuronally enriched blood-derived extracellular vesicles. Integrating evidence from these three approaches tentatively suggests for the first time that a comprehensive assessment of the brain's default mode network (DMN), combining these methodologies within a single study, may offer a useful biomarker to quantify in vivo brain-specific insulin resistance in humans. Correlating DMN responses to concentrations of pY-IRS-1 in blood-derived extracellular vesicles would corroborate evidence for a brain-specific biomarker and provide a scalable approach to detecting brain-specific insulin resistance in humans. This advancement would enable in vivo evaluations of insulin resistance in the central nervous system, akin to the precise measurements of systemic insulin resistance seen in T2DM. An established and clearly defined biomarker of in vivo brain insulin resistance in humans would permit further investigation into the links between diabetes and dementia, ultimately bolstering support for secondary dementia prevention by identifying those at higher risk for cognitive decline.</div></div>","PeriodicalId":52767,"journal":{"name":"Biomarkers in Neuropsychiatry","volume":"12 ","pages":"Article 100125"},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143593276","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A systematic review of neurobiological aspects of borderline personality disorder among adolescent patients","authors":"Liliana Cruz-Ausejo ,&nbsp;Alex Rojas-Ortega ,&nbsp;Glauco Valdivieso-Jiménez ,&nbsp;Anthony Copez-Lonzoy ,&nbsp;Andrea Matayoshi ,&nbsp;Josmel Pacheco-Mendoza ,&nbsp;Vicente A. Benites-Zapata","doi":"10.1016/j.bionps.2024.100114","DOIUrl":"10.1016/j.bionps.2024.100114","url":null,"abstract":"<div><h3>Background</h3><div>Borderline personality Disorder is a complex mental health condition with disturbances in emotions, self-perception, and relationships. Emerging in adolescence, it reaches its peak in early adulthood, impacting 1 %-3 % of individuals.</div></div><div><h3>Methods</h3><div>We documented this review in PROSPERO with the registration code CRD4202126220. Subsequently, we conducted a comprehensive search across Pubmed, PsycINFO, Medline, Embase, Web of Science and Scopus databases. A systematic synthesis focusing on the neurobiological foundations of borderline personality disorder is presented.</div></div><div><h3>Results</h3><div>A total of 22 studies and 1400 participants were included. Most of the studies 10/22 and 4/22 were from Australia and Germany, respectively. Genetic findings linked the short allele of 5-HTTLPR to the elevated borderline personality disorder traits and revealed neuroendocrine alterations. While imaging studies documented structural brain changes in areas such as the dorsolateral frontal gyrus and hippocampus, and reduced volumes in the anterior cingulate cortex and corpus callosum. Electrophysiological studies indicated abnormal cerebral maturation with diminished P300 amplitudes and increased alpha phase synchrony in borderline personality disorder adolescents, particularly during emotional tests.</div></div><div><h3>Conclusion</h3><div>We concluded that while borderline personality disorder symptoms may endure from adolescence into adulthood, existing evidence lacks consistency in neurobiological findings. Differences in the prefrontal cortex, orbitofrontal cortex, amygdala and hippocampus showed potential significance, however, electrophysiological, biochemical and genetic presented insufficient generalizable evidence for adolescents. Longitudinal studies and further investigation are needed.</div></div>","PeriodicalId":52767,"journal":{"name":"Biomarkers in Neuropsychiatry","volume":"12 ","pages":"Article 100114"},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143181180","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inducible HSP72 protein as a marker of neuronal vulnerability in brain research: A potential biomarker for clinical psychiatry?","authors":"Ana-Maria Iorgu ,&nbsp;Dragos Inta ,&nbsp;Peter Gass","doi":"10.1016/j.bionps.2025.100123","DOIUrl":"10.1016/j.bionps.2025.100123","url":null,"abstract":"<div><div>The aim of this review is to analyze the potential of the inducible form of 70-kDa heat shock protein (i.e. HSP72) as a biomarker for neuropsychiatric diseases, focusing on both animal and clinical studies. We first discuss findings from animal studies where HSP72 has already revealed its reliability as a sensitive marker of neuronal vulnerability, especially research investigating NMDAR antagonists-induced neurotoxicity, cerebral ischemia, epilepsy, behavioral stress, and effects of psychoactive and/or addictive substances. Next, we summarized human studies providing evidence for the involvement of HSP72 in the pathology of neuropsychiatric disorders like major depression, bipolar disorder, schizophrenia, attention deficit hyperactivity disorder, autism spectrum disorder, and neurodegenerative disorders. Finally, we discuss potential future research approaches needed to further investigate and possibly validate HSP72 as a biomarker in clinical psychiatry.</div></div>","PeriodicalId":52767,"journal":{"name":"Biomarkers in Neuropsychiatry","volume":"12 ","pages":"Article 100123"},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143428838","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}