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We conducted a small, open-label, pilot study of daratumumab to explore target engagement, safety, and potential efficacy in patients with mild to moderate Alzheimer's disease. Daratumumab SC 1800 mg was given subcutaneously weekly for 8 weeks, then every 2 weeks for 16 weeks. Flow cytometry to measure the CD38+ proportion of CD8 + CD4- T cells and cognitive assessments were performed at baseline, day 176, and day 246. Daratumumab significantly reduced CD38 + CD8 + CD4- T cells after 24 weeks and this effect persisted 11 weeks thereafter. There was no hematological toxicity or unexpected adverse events. Responder analysis showed no improvement on cognitive outcome measures.

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Importance: The emergence of psychotic symptoms in Alzheimer disease (AD) is associated with accelerated cognitive and functional decline that may be related to disease pathology. Objective: To investigate the longitudinal dynamics of plasma tau phosphorylated at threonine 181 (p-tau181) and neurofilament light chain protein (NfL) levels in association with the emergence of psychotic symptoms (delusions and hallucinations) in the context of AD. Design, Setting, and Participants: This cohort study used longitudinal data from the Alzheimer Disease Neuroimaging Initiative (ADNI). Baseline analyses compared patients with mild cognitive impairment (MCI) and AD (both with psychosis [AD+P] and without psychosis [AD-P]) and participants who were cognitively unimpaired (CU). For the longitudinal analysis, participants with MCI and AD were subdivided into patients with evidence of psychosis at baseline (AD+P baseline) and patients free of psychosis at baseline who showed incidence of psychosis over the course of the study (AD+P incident). Study data were analyzed between June and November 2023. Exposures: Plasma p-tau181 and NfL measures in individuals with MCI and AD, both with and without psychosis. Main Outcomes and Measures: Plasma p-tau181 and NfL quantifications up to 48 months and concurrent assessments of presence or absence of delusions and hallucinations via the Neuropsychiatric Inventory (NPI) questionnaire. Results: The cohort included 752 participants with AD (mean [SD] age, 74.2 [7.7] years; 434 male [57.7%]). A total of 424 CU participants had a mean (SD) age of 75.4 (6.6) years of whom 222 were female (52.4%). In the longitudinal analysis of p-tau181 trajectories of the AD+P group, the group of patients who showed incidence of psychosis over the course of follow-up (AD+P incident) demonstrated an associated increase in plasma p-tau181 levels compared with the group of patients who had psychosis at baseline (AD+P baseline) and showed an associated decrease in plasma p-tau181 levels (F4, 117 = 3.24; P = .01). The mean slope of p-tau181 change was significantly different in AD+P incident and AD+P baseline groups (F5,746 = 86.76, P < .0001) and when only individuals with amyloid-ß positivity (Aß+), which was determined using positron emission tomography, were compared (F5,455 = 84.60, P < .001). Patients who experienced psychosis at any time had increased levels of NfL relative to those who never experienced psychosis. Conclusions and Relevance: Results of this cohort study suggest that the emergence of psychosis in AD was associated with elevations in plasma levels of p-tau181, highlighting the potential utility of plasma p-tau181 as a biomarker of neuropsychiatric illness in AD, which could have implications for predictive and treatment response strategies.

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The CACNA1C and the ZNF804A genes are among the most relevant schizophrenia GWAS findings. Recent evidence shows that the interaction of these genes with the schizophrenia diagnosis modulates brain functional response to a verbal fluency task. To better understand how these genes might influence the risk for schizophrenia, we aimed to study the interplay between CACNA1C and ZNF804A on working memory brain functional correlates. The analyses included functional and behavioural N-back task data (obtained from an fMRI protocol) and CACNA1C-rs1006737 and ZNF804A-rs1344706 genotypes for 78 healthy subjects and 78 patients with schizophrenia (matched for age, sex and premorbid IQ). We tested the effects of the epistasis between these genes as well as of the three-way interaction (CACNA1C × ZNAF804A × diagnosis) on working memory-associated activity (N-back: 2-back vs 1-back). We detected a significant CACNA1C × ZNAF804A interaction on working memory functional response in regions comprising the ventral caudate medially and within the left hemisphere, the superior and inferior orbitofrontal gyrus, the superior temporal pole and the ventral-anterior insula. The individuals with the GWAS-identified risk genotypes (CACNA1C-AA/AG and ZNF804A-AA) displayed a reduced working memory modulation response. This genotypic combination was also associated with opposite brain activity patterns between patients and controls. While further research will help to comprehend the neurobiological mechanisms of this interaction, our data highlight the role of the epistasis between CACNA1C and ZNF804A in the functional mechanisms underlying the pathophysiology of schizophrenia.

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The KCNH2 gene, encoding for a subunit of a voltage-gated potassium channel, has been identified as a key element of neuronal excitability and a promising novel therapeutic target for schizophrenia (SZ). Nonetheless, evidence highlighting the role of KCNH2 on cognitive and brain activity phenotypes comes mainly from studies based on healthy controls (HC). Therefore, we aimed to study the role of KCNH2 on the brain functional differences between patients with SZ and HC. The fMRI sample comprised 78 HC and 79 patients with SZ (matched for age, sex and premorbid IQ). We studied the effect of the polymorphism KCNH2-rs3800779 on attention and working memory-related brain activity, evaluated through the N-back task, in regions with detected diagnostic differences (regression model, controlled for age, sex and premorbid IQ, FEAT-FSL). We report a significant diagnosis x KCNH2 interaction on brain activity (1-back vs baseline contrast) at the medial superior prefrontal cortex (Zmax=3.55, p = 0.00861). In this region, patients with SZ carrying the risk genotype (AA) show a deactivation failure, while HC depict the opposite pattern towards deactivation. The brain region with significant diagnosis x KCNH2 interaction has been previously associated with SZ. The results of this study, in which the role of KCNH2 on fMRI response is analysed for the first time in patients, suggest that KCNH2 variability contributes to inefficient brain activity modulation during the N-back task in affected subjects. These data may pave the way to further understand how KCNH2 genetic variability is related to the pathophysiological mechanisms underlying schizophrenia.

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INTRODUCTION: Psychosis in Alzheimer's disease (AD) is associated with grave clinical consequences including a precipitous cognitive decline and a hastened demise. These outcomes are aggravated by use of existing antipsychotic medications, which are also associated with cognitive decline and increased mortality; preclinical models that would develop new therapeutic approaches are desperately needed. The current report evaluates the ability of the neoteric antipsychotic, pimavanserin, to normalize hyperkinesis and sensorimotor gating in the novel catechol-O-methyltransferase (COMT) deleted P301L/COMT- and rTg(P301L)4510 models of psychotic AD, and the impact of pimavanserin on tau pathology. METHODS: Female P301L/COMT- mice were behaviorally characterized for abnormalities of locomotion and sensorimotor gating, and biochemically characterized for patterns of tau phosphorylation relative to relevant controls utilizing high-sensitivity tau enzyme-linked immunosorbent assay (ELISA). Female P301L/COMT- and rTg(P301L)4510 mice were randomized to pimavanserin or vehicle treatment to study the ability of pimavanserin to normalize locomotion and rescue sensorimotor gating. Additionally, high-sensitivity tau ELISA was used to investigate the impact of treatment on tau phosphorylation. RESULTS: P301L/COMT- mice evidenced a hyperlocomotive phenotype and deficits of sensorimotor gating relative to wild-type mice on the same background, and increased tau phosphorylation relative to COMT-competent P301L mice. Pimavanserin normalized the hyperkinetic phenotype in both the P301L/COMT- and rTg(P301L)4510 mice but had no impact on sensorimotor gating in either model. Pimavanserin treatment had little impact on tau phosphorylation patterns. DISCUSSION: These data suggest that pimavanserin ameliorates tau-driven excessive locomotion. Given the morbidity associated with aberrant motor behaviors such as pacing in AD and lack of effective treatments, future studies of the impact of pimavanserin on actigraphy in patients with this syndrome may be warranted.

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Deficits in emotion processing are a core feature of schizophrenia, but their neurobiological bases are poorly understood. Previous research, mainly focused on emotional face processing and emotion recognition deficits, has shown controverted results. Furthermore, the use of faces has been questioned for not entailing an appropriate stimulus to study emotional processing. This highlights the importance of investigating emotional processing abnormalities using evocative stimuli. For the first time, we have studied the brain responses to scenic stimuli in patients with schizophrenia. We selected scenes from the IAPS that elicit fear, disgust, happiness, and sadness. Twenty-six patients with schizophrenia and thirty age-, sex- and premorbid IQ-matched healthy controls were included. Behavioral task results show that patients tended to misclassify disgust and sadness as fear. Brain responses in patients were different from controls in images eliciting disgust and fear. In response to disgust images, patients hyperactivated the right temporal cortex, which was not activated by the controls. With fear images, hyperactivation was observed in brain regions involved in fear processing, including midline regions from the medial frontal cortex to the anterior cingulate cortex, the superior frontal gyrus, inferior and superior temporal cortex, and visual areas. These results suggest that schizophrenia is characterized by hyper-responsivity to stimuli evoking high-arousal, negative emotions, and a bias towards fear in emotion recognition.

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Schizophrenia is a complex psychiatric disorder that displays an outstanding interindividual variability in clinical manifestation and neurobiological substrates. A better characterization and quantification of this heterogeneity could guide the search for both common abnormalities (linked to lower intersubject variability) and the presence of biological subtypes (leading to a greater heterogeneity across subjects). In the current study, we address interindividual variability in functional connectome by means of resting-state fMRI in a large sample of patients with schizophrenia and healthy controls. Among the different metrics of distance/dissimilarity used to assess variability, geodesic distance showed robust results to head motion. The main findings of the current study point to (i) a higher between subject heterogeneity in the functional connectome of patients, (ii) variable levels of heterogeneity throughout the cortex, with greater variability in frontoparietal and default mode networks, and lower variability in the salience network, and (iii) an association of whole-brain variability with levels of clinical symptom severity and with topological properties of brain networks, suggesting that the average functional connectome overrepresents those patients with lower functional integration and with more severe clinical symptoms. Moreover, after performing a graph theoretical analysis of brain networks, we found that patients with more severe clinical symptoms had decreased connectivity at both whole-brain level and within the salience network, and that patients with higher negative symptoms had large-scale functional integration deficits.

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OBJECTIVES: The profiles of cortical abnormalities in schizophrenia and bipolar disorder, and how far they resemble each other, have only been studied to a limited extent. The aim of this study was to identify and compare the changes in cortical morphology associated with these pathologies. METHODS: A total of 384 subjects, including 128 patients with schizophrenia, 128 patients with bipolar disorder and 127 sex-age-matched healthy subjects, were examined using cortical surface-based morphology. Four cortical structural measures were studied: cortical volume (CV), cortical thickness (CT), surface area (SA) and gyrification index (GI). Group comparisons for each separate cortical measure were conducted. RESULTS: At a threshold of P = 0.05 corrected, both patient groups showed significant widespread CV and CT reductions in similar areas compared to healthy subjects. However, the changes in schizophrenia were more pronounced. While CV decrease in bipolar disorder was exclusively explained by cortical thinning, in schizophrenia it was driven by changes in CT and partially by SA. Reduced GI was only found in schizophrenia. The direct comparison between both disorders showed significant reductions in all measures in patients with schizophrenia. CONCLUSIONS: Cortical volume and cortical thickness deficits are shared between patients with schizophrenia and bipolar disorder, suggesting that both pathologies may be affected by similar environmental and neurodegenerative factors. However, the exclusive alteration in schizophrenia of metrics related to the geometry and curvature of the brain cortical surface (SA, GI) suggests that this group is influenced by additional neurodevelopmental and genetic factors.

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Editorial of vol. 31, n. 2.

Editorial del vol. 31, nº 2.

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INTRODUCTION: The extent of working memory (WM) and executive function (EF) impairment in mild cognitive impairment (MCI) is not well-characterized. METHODS: We compared 48 patients with MCI, 124 noncognitively impaired elderly healthy controls, and 57 patients with Alzheimer's disease (AD) on multiple WM/EF measures, frontal lobe integrity indexes, and functioning. RESULTS: Patients with MCI demonstrated worse performance on nearly all WM/EF tests. This profile of impairment was refined in a factor analysis that identified three primary WM/EF constructs: WM storage; speed and controlled visual search; and manipulation of information and problem solving. EF impairments were associated with reductions in prefrontal cortical thickness. WM/EF accounted for over 50% of the variance in functional competence. DISCUSSION: In MCI, WM/EF impairments are far from rare, based on specific compromises to frontal cortex circuitry, and are associated with loss of everyday functioning. WM/EF impairments, even at this potentially prodromal stage of AD, have clinically deleterious consequences.

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Introducción: Los síntomas negativos prevalecen en la esquizofrenia y están asociados con un peor resultado. La validación de nuevos instrumentos psicométricos podría contribuir a una mejor evaluación de los síntomas negativos y a un avance en su tratamiento. La escala de evaluación de los síntomas negativos-16 (Negative Symptom Assessment-16 [NSA-16]) ha demostrado adecuadas propiedades psicométricas, pero existe la necesidad de validarla en otros idiomas diferentes del inglés. Este estudio tiene como objetivo examinar las propiedades psicométricas de la versión española de la NSA-16 (Sp-NSA-16). Material y método: Estudio observacional, transversal de validación en una muestra de 123 pacientes con diagnóstico de esquizofrenia en tratamiento ambulatorio. Evaluación: NSA-16, PANSS, HDRS, ICG-ESQ y PSP. Resultados: Los resultados muestran unas adecuadas propiedades psicométricas, alta consistencia interna (alfa de Cronbach=0,86), validez convergente (escala negativa de la PANSS, factor negativo de Marder de la PANSS y escala de los síntomas negativos de la ICG: valores r entre 0,81 y 0,94) y validez divergente (escala positiva de la PANSS y HDRS: valores r entre 0,10 y 0,34). Además, la NSA-16 también muestra validez discriminante (curva ROC=0,97; IC 95%=0,94 a 1,00; 94,3% de sensibilidad y 83,3% de especificidad). Conclusiones: La Sp-NSA-16 es fiable y válida para medir los síntomas negativos en pacientes con esquizofrenia. Proveemos a los clínicos españoles con una nueva herramienta para la práctica clínica e investigación. Sin embargo, es necesario proporcionar más información sobre su fiabilidad interevaluadores

Introduction: Negative symptoms are prevalent in schizophrenia and associated with a poorer outcome. Validated newer psychometric instruments could contribute to better assessment and improved treatment of negative symptoms. The Negative Symptom Assessment-16 (NSA-16) has been shown to have strong psychometric properties, but there is a need for validation in non-English languages. This study aimed to examine the psychometric properties of a Spanish version of the NSA-16 (Sp-NSA-16). Material and method: Observational, cross-sectional validation study in a sample of 123 outpatients with schizophrenia. Assessments: NSA-16, PANSS, HDRS, CGI-SCH and PSP. Results: The results indicate appropriate psychometric properties, high internal consistency (Cronbach's alpha=0.86), convergent validity (PANSS negative scale, PANSS Marder Negative Factor and CGI-negative symptoms r values between 0.81 and 0.94) and divergent validity (PANSS positive scale and the HDRS r values between 0.10 and 0.34). In addition, the NSA-16 also exhibited discriminant validity (ROC curve=0.97, 95% CI=0.94 to 1.00; 94.3% sensitivity and 83.3% specificity). Conclusions: The Sp-NSA-16 is reliable and valid for measuring negative symptoms in patients with schizophrenia. This provides Spanish clinicians with a new tool for clinical practice and research. However, it is necessary to provide further information about its inter-rater reliability

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Aim: To analyze age-related cerebral blood flow (CBF) using arterial spin labeling (ASL) MRI in healthy subjects with multivariate principal component analysis (PCA). Methods: 50 healthy subjects (mean age 45.8 ± 18.5 years, range 21-85) had 3D structural MRI and pseudo-continuous ASL MRI at resting state. The relationship between CBF and age was examined with voxel-based univariate analysis using multiple regression and two-sample t-test (median age 41.8 years as a cut-off). An age-related CBF pattern was identified using multivariate PCA. Results: Age correlated negatively with CBF especially anteriorly and in the cerebellum. After adjusting by global value, CBF was relatively decreased with aging in certain regions and relatively increased in others. The age-related CBF pattern showed relative reductions in frontal and parietal areas and cerebellum, and covarying increases in temporal and occipital areas. Subject scores of this pattern correlated negatively with age (R2 = 0.588; P < 0.001) and discriminated between the older and younger subgroups (P < 0.001). Conclusion: A distinct age-related CBF pattern can be identified with multivariate PCA using ASL MRI.

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INTRODUCTION: Negative symptoms are prevalent in schizophrenia and associated with a poorer outcome. Validated newer psychometric instruments could contribute to better assessment and improved treatment of negative symptoms. The Negative Symptom Assessment-16 (NSA-16) has been shown to have strong psychometric properties, but there is a need for validation in non-English languages. This study aimed to examine the psychometric properties of a Spanish version of the NSA-16 (Sp-NSA-16). MATERIAL AND METHOD: Observational, cross-sectional validation study in a sample of 123 outpatients with schizophrenia. ASSESSMENTS: NSA-16, PANSS, HDRS, CGI-SCH and PSP. RESULTS: The results indicate appropriate psychometric properties, high internal consistency (Cronbach's alpha=0.86), convergent validity (PANSS negative scale, PANSS Marder Negative Factor and CGI-negative symptoms r values between 0.81 and 0.94) and divergent validity (PANSS positive scale and the HDRS r values between 0.10 and 0.34). In addition, the NSA-16 also exhibited discriminant validity (ROC curve=0.97, 95% CI=0.94 to 1.00; 94.3% sensitivity and 83.3% specificity). CONCLUSIONS: The Sp-NSA-16 is reliable and valid for measuring negative symptoms in patients with schizophrenia. This provides Spanish clinicians with a new tool for clinical practice and research. However, it is necessary to provide further information about its inter-rater reliability.

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INTRODUCTION: Episodic memory processes are supported by different subregions of the medial temporal lobe (MTL). In contrast to a unitary model of memory recognition supported solely by the hippocampus, a current model suggests that item encoding engages perirhinal cortex, whereas relational encoding engages parahippocampal cortex and the hippocampus. However, this model has not been examined in the context of aging, neurodegeneration, and MTL morphometrics. METHODS: Forty-four healthy subjects (HSs) and 18 cognitively impaired subjects (nine mild cognitive impairment [MCI] and nine Alzheimer's disease [AD] patients) were assessed with the relational and item-specific encoding task (RISE) and underwent 3T magnetic resonance imaging. The RISE assessed the differential contribution of relational and item-specific memory. FreeSurfer was used to obtain measures of cortical thickness of MTL regions and hippocampus volume. RESULTS: Memory accuracies for both item and relational memory were significantly better in the HS group than in the MCI/AD group. In MCI/AD group, relational memory was disproportionately impaired. In HSs, hierarchical regressions demonstrated that memory was predicted by perirhinal thickness after item encoding, and by hippocampus volume after relational encoding (both at trend level) and significantly by parahippocampal thickness at associative recognition. The same brain morphometry profiles predicted memory accuracy in MCI/AD, although more robustly perirhinal thickness for item encoding (R2 = 0.31) and hippocampal volume and parahippocampal thickness for relational encoding (R2 = 0.31). DISCUSSION: Our results supported a model of episodic memory in which item-specific encoding was associated with greater perirhinal cortical thickness, while relational encoding was associated with parahippocampal thickness and hippocampus volume. We identified these relationships not only in HSs but also in individuals with MCI and AD. In the subjects with cognitive impairment, reductions in hippocampal volume and impairments in relational memory were especially prominent.

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BACKGROUND: The Relational and Item-Specific Encoding task (RISE) measures episodic memory subcomponents, including item-specific and relational encoding of to-be-remembered stimuli. These memory components are neurobiologically relevant because they may engage distinct subregions of the medial temporal lobe, perirhinal and entorhinal cortices, parahippocampus, and hippocampus. METHODS: A total of 125 participants, including 84 healthy controls (HC), 22 mild cognitive impairment-diagnosed and 19 Alzheimer disease (AD)-diagnosed participants, were administered the RISE and neuropsychological measures. Stepwise linear regressions assessed prediction of functional ability from RISE d' measures. ANOVAs and logistic regressions determined the ability of the RISE to discriminate between the diagnostic groups. In addition, the psychometric properties of the RISE were examined. RESULTS: RISE measures predicted diagnosis with pseudo R2 values in the range of 0.25-0.30. Receiver operating characteristic curves demonstrated adequate sensitivity and specificity with areas under the curve in the range of 0.78-0.98. Memory following relational encoding was a significant predictor of everyday functional competence. The RISE had acceptable psychometric properties, with the exception of floor effects in the AD group. CONCLUSION: The RISE measures significantly predicted diagnosis and predicted everyday functional competence. The RISE offers unique advantages in the assessment of HC and individuals with preclinical AD.

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Compromises in compensatory neurobiologic mechanisms due to aging and/or genetic factors (i.e., APOE gene) may influence brain-derived neurotrophic factor (BDNF) val66met polymorphism effects on temporal lobe morphometry and memory performance. We studied 2 cohorts from Alzheimer's Disease Neuroimaging Initiative: 175 healthy subjects and 222 with prodromal and established Alzheimer's disease. Yearly structural magnetic resonance imaging and cognitive performance assessments were carried out over 3 years of follow-up. Both cohorts had similar BDNF Val/Val and Met allele carriers' (including both Val/Met and Met/Met individuals) distribution. In healthy subjects, a significant trend for thinner posterior cingulate and precuneus cortices was detected in Met carriers compared to Val homozygotes in APOE E4 carriers, with large and medium effect sizes, respectively. The mild cognitive impairment/Alzheimer's disease cohort showed a longitudinal decline in entorhinal thickness in BDNF Met carriers compared to Val/Val in APOE E4 carriers, with effect sizes ranging from medium to large. In addition, an effect of BDNF genotype was found in APOE E4 carriers for episodic memory (logical memory and ADAS-Cog) and semantic fluency measures, with Met carriers performing worse in all cases. These findings suggest a lack of compensatory mechanisms in BDNF Met carriers and APOE E4 carriers in healthy and pathological aging.

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BACKGROUND: The earliest stage of preclinical Alzheimer's disease (AD) is defined by low levels of cerebrospinal fluid (CSF) amyloid-ß (Aß42). However, covariance in longitudinal dynamic change of Aß42 and tau in incipient preclinical AD is poorly understood. OBJECTIVE: To examine dynamic interrelationships between Aß42 and tau in preclinical AD. METHODS: We followed 47 cognitively intact participants (CI) with available CSF data over four years in ADNI. Based on longitudinal Aß42 levels in CSF, CI were classified into three groups: 1) Aß42 stable with normal levels of Aß42 over time (n = 15); 2) Aß42 declining with normal Aß42 levels at baseline but showing decline over time (n = 14); and 3) Aß42 levels consistently abnormal (n = 18). RESULTS: In the Aß42 declining group, suggestive of incipient preclinical AD, CSF phosphorylated tau (p-tau) showed a similar longitudinal pattern of increasing abnormality over time (p = 0.0001). Correlation between longitudinal slopes of Aß42 and p-tau confirmed that both trajectories were anti-correlated (rho = -0.60; p = 0.02). Regression analysis showed that Aß42 slope (decreasing Aß42) predicted p-tau slope (increasing p-tau) (R2 = 0.47, p = 0.03). Atrophy in the hippocampus was predicted by the interaction of Aß42 and p-tau slopes (p <  0.0001) only in this incipient preclinical AD group. In all groups combined, memory decline was predicted by p-tau. CONCLUSIONS: The evolution of Aß42 and p-tau CSF biomarkers in CI subjects follows an anti-correlated trajectory, i.e., as Aß42 declined, p-tau increased, and thus was suggestive of strong temporal coincidence. Rapid pathogenic cross-talk between Aß42 and p-tau thus may be evident in very early stages of preclinical AD.

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The effectiveness of cognitive remediation therapy (CRT) for the neuropsychological deficits seen in schizophrenia is supported by meta-analysis. However, a recent methodologically rigorous trial had negative findings. In this study, 130 chronic schizophrenic patients were randomly assigned to computerized CRT, an active computerized control condition (CC) or treatment as usual (TAU). Primary outcome measures were 2 ecologically valid batteries of executive function and memory, rated under blind conditions; other executive and memory tests and a measure of overall cognitive function were also employed. Carer ratings of executive and memory failures in daily life were obtained before and after treatment. Computerized CRT was found to produce improvement on the training tasks, but this did not transfer to gains on the primary outcome measures and most other neuropsychological tests in comparison to either CC or TAU conditions. Nor did the intervention result in benefits on carer ratings of daily life cognitive failures. According to this study, computerized CRT is not effective in schizophrenia. The use of both active and passive CCs suggests that nature of the control group is not an important factor influencing results.

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