Anxiety disorders are highly prevalent yet lack objective biomarkers. Whereas threat-related attentional biases are well documented, less is known about broader eye movement alterations that may characterise anxiety.

To characterise multi-paradigm eye movement profiles in anxiety disorders and evaluate their potential as behavioural markers for disorder differentiation.

Eye movements were recorded in 91 patients with anxiety disorders, 118 with depressive disorders and 98 healthy controls during free viewing of neutral-stimuli, smooth-pursuit and fixation-stability tasks. Principal component analysis was applied to derive latent eye movement dimensions, which were then tested for group differences, associations with symptom severity and classification performance.

Compared with both patients with depression and healthy controls, patients with anxiety disorders exhibited hyper-scanning during free viewing, characterised by increased saccade frequency and path length, and hyper-pursuit during smooth pursuit, reflected in increased velocity gain, fewer intrusive saccades and more catch-up saccades. Principal component analysis identified six latent components, among which active visual exploration, pupillary arousal and smooth-pursuit control demonstrated robust group differences. Machine learning models trained on 6 components yielded areas under the receiver operating characteristic curve of 0.82 for anxiety versus healthy controls, 0.83 for depression versus healthy controls and 0.61 for anxiety versus depression.

Hyper-scanning and hyper-pursuit emerge as defining eye movement signatures of anxiety, linking core mechanisms of vigilance and prediction with measurable behavioural markers. These insights position eye-tracking as a promising behavioural modality for mechanism-informed differentiation across affective disorders.

Associations of cerebrospinal fluid biomarkers with sleep, functionality and the MDS-UPDRS in dementia with Lewy bodies (DLB) and late-onset Alzheimer’s disease (AD) help elucidate their pathophysiological underpinnings.

Consecutive outpatients with DLB and AD were matched by sex, cognitive scores and dementia stage, along with cognitively healthy controls matched by age and sex to investigate associations of cerebrospinal fluid amyloid-β (Aβ42,Aβ40,Aβ38), tau, phospho-tauThr181, ubiquitin, α-synuclein and neurofilament light (NfL) with sleep duration, Schwab & England scale and MDS-UPDRS, adjusted for sex, age and APOE-ϵ4 alleles.

Patients with DLB (APOE-ϵ4+:n=11, 76.64±9.0years; APOE-ϵ4-:n=16, 79.75±9.0years) were paired with patients with AD (APOE-ϵ4+:n=12, 80.17±5.7years; APOE-ϵ4-:n=15, 81.67±5.9years) and controls (APOE-ϵ4+:n=4, 82.00±6.4years; APOE-ϵ4-:n=23, 77.87±9.0years); two-thirds were women. APOE-ϵ4 carriers with dementia had more amyloidosis, higher phospho-tauThr181/Aβ42 and α-synuclein/Aβ42. In DLB, APOE-ϵ4 non-carriers had lower Schwab & England scores and higher MDS-UPDRS-I&II scores, lower tau/phospho-tauThr181 and higher ubiquitin and NfL than APOE-ϵ4 carriers. In controls, APOE-ϵ4 non-carriers had lower Aβ42 and Aβ42/Aβ38, higher phospho-tauThr181/Aβ42 and α-synuclein/Aβ42 than APOE-ϵ4 carriers. In DLB, sleep duration was associated with Aβ38 and α-synuclein and inversely associated with tau/phospho-tauThr181 and tau/ubiquitin; Schwab & England scores were associated with tau/ubiquitin and inversely associated with tau/phospho-tauThr181; MDS-UPDRS-I&II was associated with Aβ42/Aβ38; MDS-UPDRS-III was associated with tau/phospho-tauThr181; MDS-UPDRS-V ON was associated with Aβ42 and Aβ42/Aβ40, and MDS-UPDRS-V OFF was associated with Aβ42, Aβ42/Aβ40 and Aβ42/Aβ38. In AD, MDS-UPDRS-III was associated with ubiquitin.

Biomarker ratios were superior to isolated biomarkers in associations with motor and non-motor experiences in DLB, though not so prominently in AD due to less motor impairment.

Circulating tumour cells (CTCs) are unique cells that originate from the main tumor site. They circulate in the bloodstream, and are implicated in metastasis, immune evasion and recurrence in various cancers. Associated biomarkers of importance for CTC detection include epithelial cell adhesion molecule (EpCAM), human epidermal growth factor receptor 2 (HER2), programmed death ligand-1 (PD-L1), cluster of differentiation 45 (CD45) and other cancer-specific biomolecules. Their roles as standalone biomarkers, have been thoroughly examined in CTC detection, isolation and targeting.

This review collates key findings on CTC characteristics and biomarker identification. The most recent CTC isolation and detection technologies are discussed, along with individual approaches based on inclusion and exclusion of cell-specific biomarkers. Emerging treatments integrating CTCs, including nanocarrier-mediated drug delivery, have been analyzed. We have discussed both the physical and research barriers in the current landscape.

Recent advances have determined that such biomarkers are more reliable when associated with secondary biomarkers, due to concerns regarding immune evasion and low sensitivity. The identification of these molecules has fast-tracked the development of several groundbreaking technologies.

The prognostic and predictive role of CTCs in various cancers revealed promising results. The development of integrative therapeutics can enhance patient survival and quality of life. These advancements depend on addressing key issues, such as molecular characterization and low abundance of CTCs.

Early detection of respiratory decline is crucial in amyotrophic lateral sclerosis (ALS). We tested if nocturnal polysomnography (PSG) predicts dyspnea onset in mild ALS patients with preserved daytime function.

In this study, 41 mild ALS patients (ALS Functional Rating Scale-Revised [ALSFRS-R] ≥ 37, sitting forced vital capacity [FVC] ≥80% predicted, no dyspnea) and 41 matched controls underwent baseline assessment, including ALSFRS-R scoring, pulmonary function tests, and overnight PSG. ALS patients were followed for 12 months. Baseline apnea–hypopnea index (AHI) and oxygen saturation (mean SpO2, minimum SpO2) were analyzed as continuous predictors and using exploratory thresholds (AHI ≥ 5 events/h, min SpO2 ≤ 88%, mean SpO2 ≤ 95%) for dyspnea onset (Dyspnea-ALS-15 [DALS-15] > 0).

Compared to controls, ALS patients had significantly higher AHI (p = 0.004) and lower minimum SpO2 (p = 0.018). The ALSFRS-R orthopnea subscore showed a significant positive correlation with mean and minimum SpO2 (P < 0.05). Cox regression identified baseline AHI (HR 1.08 per event/h; 95% CI 1.01–1.15, p = 0.028) and minimum SpO2 (HR 0.94 per %; 95% CI 0.88–0.99, p = 0.033) as independent predictors of dyspnea onset within 12 months. Thresholds AHI ≥ 5 (HR 2.28, p = 0.031) and min SpO2 ≤ 88% (HR 2.42, p = 0.027) also predicted increased risk. Patients meeting ≥1 threshold (n = 25/37) showed trends toward greater FVC and ALSFRS-R decline.

In patients with mild ALS and normal daytime function, specific nocturnal PSG parameters (AHI, minimum SpO2) predicted the risk of dyspnea within 12 months. This longitudinal study provides novel evidence that PSG could identify early respiratory vulnerability in the incipient stage, earlier than conventional FVC-based monitoring, supporting its potential utility in refining early intervention strategies. Validation in larger cohorts is warranted.

Young-onset dementia (YOD), defined by symptom onset before age 65, encompasses diverse aetiologies and presents with prominent neuropsychiatric symptoms (NPS) that often accompany or exacerbate cognitive decline. However, the pathological mechanisms linking NPS, cognition, and biomarkers remain unclear. It was hypothesised that relationships between NPS and cognition would be mediated or moderated by cerebrospinal fluid (CSF) biomarker levels in individuals with YOD.

This retrospective, cross-sectional study included 46 participants with YOD (24 with Alzheimer’s disease [AD], 22 with non-AD dementias) diagnosed at the Neuropsychiatry Centre, Royal Melbourne Hospital. NPS were measured using the Depression Anxiety and Stress Scale and Cambridge Behavioural Inventory-Revised. Cognition was assessed using standardised neuropsychological assessments. CSF amyloid-β (Aβ42), phosphorylated tau 181 (P-tau181), total tau (T-tau), and neurofilament light chain protein (NfL) were analysed. General linear models (GLMs) examined associations between biomarkers, cognition, and NPS.

Higher P-tau181 (unstandardised beta [B] = −0.10, 95% confidence interval = [−0.20, −0.01]) and T-tau (B = −0.06 [−0.13, −0.01]) levels were associated with poorer memory recall in participants with YOD. In non-AD dementias, higher T-tau levels predicted greater NPS severity (B = 0.76 [0.06, 3.52]). NfL showed no significant associations with NPS or cognition.

Tau-related neurodegeneration (P-tau181 and T-tau) appears more closely linked to memory impairment in YOD than axonal injury markers such as NfL. In non-AD dementias, T-tau was additionally associated with behavioural symptom severity, suggesting tau-related mechanisms across subtypes. These associations require validation in larger, longitudinal, and multimodal studies to clarify temporal and mechanistic pathways.

There is no recognised cure or specific biomarker for autism spectrum disorder (ASD). Exosomes are small vesicles that carry proteins, lipids and nucleic acids. They have been investigated for diseases such as Parkinson’s and Alzheimer’s. As the conclusions were on the biological utility of exosomes as a non-invasive brain biopsy, some animal, human and in vitro exosome studies have also been presented in the ASD field. The purpose of this review is to compile the studies that have established a relationship between ASD and exosomes so far and discuss their potential for linking the gap between the laboratory and clinic.

In this systematic review, 31 PubMed articles were identified using the keywords ‘exosomal’, ‘exosome and ‘autism spectrum disorder’. After excluding 16 reviews, 4 irrelevant studies and 1 preprint, and adding 5 relevant articles, 15 research articles were included based on PRISMA criteria. The articles were investigated and reviewed by both authors. Their methodology and results are also discussed according to two main streams in studies.

Numerous studies have identified potential biomarkers, including mitochondrial DNA (mtDNA7S), cytokines including IL-1β, TNF-α and IL-6, and different types of RNAs by comparing the exosomal contents of ASD patients or models with controls. In studies that focused on treatment, behavioural improvements were shown in ASD model mice.

Since there are presently no reliable biomarkers or effective treatments for ASD, exosome-based research offers a promising avenue for early diagnosis and the creation of tailored therapies.

Contrary to the negative acute-phase protein (APP) response, there is no consistent correlation between serum pentameric C-reactive protein (pCRP) and major depression (MDD). Monomeric CRP (mCRP), a dissociation product of pCRP under immune-inflammatory conditions, exhibits pro-inflammatory effects; however, it has not been investigated in MDD or its subtypes, major dysmood disorder (MDMD) and simple dysmood disorder (SDMD).

To examine serum mCRP, albumin, transferrin, M1 macrophage and Thelper-17 immune profiles, and adverse childhood experiences (ACEs) in MDD, MDMD and SDMD.

Seventy-nine MDMD patients, 30 SDMD patients, and 40 controls were included. Serum mCRP was measured by ELISA; albumin, transferrin, and pCRP by biochemical assays; and cytokines using Luminex technology.

MDMD patients showed significantly higher mCRP compared with SDMD and controls, while both patient groups exhibited reduced albumin and transferrin. Combining mCRP with albumin and transferrin showed an adequate accuracy for MDD (area under the ROC Curve = 0.793). Adding IL-17A and ACEs improved accuracy (ROC = 0.855). Serum mCRP levels are additionally associated with pCRP, M1 macrophage profile, body mass index, and ACEs. Up to 36.6% of the variance in overall severity of depression was explained by mCRP, T-helper-17 profile, ACEs (all positively), albumin and transferrin (both inversely).

Future research in MDD should employ mCRP rather than pCRP as a biomarker of depression/MDMD. Combining mCRP with biomarkers of the negative acute-phase response identified 63.7% of MDD patients with a smouldering acute-phase response, with a specificity of 82.1%. We recommend to assess mCRP rather than pCRP in MDD studies.