To explore the capability of the amide-proton-transfer weighted (APTW) magnetic resonance imaging (MRI) in the evaluation of clinical neurological deficit at the time of hospitalization and assessment of long-term daily functional outcome for patients with acute ischemic stroke (AIS). We recruited 55 AIS patients with brain MRI acquired within 24–48 h of symptom onset and followed up with their 90-day modified Rankin Scale (mRS) score. APT weighted MRI was performed for all the study subjects to measure APTW signal quantitatively in the acute ischemic area (APTW_ipsi) and the contralateral side (APTW_cont). Change of the APT signal between the acute ischemic region and the contralateral side (ΔAPTW) was calculated. Maximum APTW signal (APTW_max) and minimal APTW signal (APTW_min) were also acquired to demonstrate APTW signals heterogeneity (APTW_max−min). In addition, all the patients were divided into 2 groups according to their 90-day mRS score (good prognosis group with mRS score <2 and poor prognosis group with mRS score ≥2). In the meantime, ΔAPTW of these groups was compared. We found that ΔAPTW was in good correlation with National Institutes of Health Stroke Scale (NIHSS) score (R² = 0.578, p < 0.001) and 90-day mRS score (R² = 0.55, p < 0.001). There was significant difference of ΔAPTW between patients with good prognosis and patients with poor prognosis. Plus, APTW_max−min was significantly different between two groups. These results suggested that APT weighted MRI could be used as an effective tool to assess the stroke severity and prognosis for patients with AIS, with APTW signal heterogeneity as a possible biomarker.

Positron emission tomography (PET) probes are specific and sensitive while suffering from radiation risk. It is worthwhile to explore the chemical emission saturation transfer (CEST) effects of the probe prototypes and repurpose them for CEST imaging to avoid radiation. In this study, we used ¹¹C-PiB as an example of a PET probe for detecting amyloid and tested the feasibility of repurposing this PET probe prototype, PiB, for CEST imaging. After optimizing the parameters through preliminary phantom experiments, we used APP/PS1 transgenic mice and age-matched C57 mice for in vivo CEST magnetic resonance imaging (MRI) of amyloid. Furthermore, the pathological assessment was conducted on the same brain slices to evaluate the correlation between the CEST MRI signal abnormality and β-amyloid deposition detected by immunohistochemical staining. In our results, the Z-spectra revealed an apparent CEST effect that peaked at approximately 6 ppm. APP/PS1 mice as young as 9 months injected with PiB showed a significantly higher CEST effect compared to the control groups. The hyperintense region was correlated with the Aβ deposition shown by pathological staining. In conclusion, repurposing the PET probe prototype for CEST MRI imaging is feasible and enables label- and radiation-free detection of the amyloid while maintaining the sensitivity and specificity of the ligand. This study opens the door to developing CEST probes based on PET probe prototypes.

Cancer-associated fibroblasts (CAFs) are essential components of the tumor microenvironment. Fibroblast activation protein (FAP) is overexpressed in CAFs. FAP-targeted molecular imaging agents, including the FAP inhibitors (FAPIs), have shown promising results in tumor diagnosis. We aimed to design a Gd-labeled FAPI Dimer, Gd-DOTA-Suc-Lys-(FAPI04)₂, to optimize the pharmacokinetics and evaluate its potential capacity for targeting FAP-positive solid tumors in vivo. The Gd-labeled FAPI Dimer was successfully synthesized with exceeding 98% purity. Preclinical pharmacokinetics were determined in assessed FAP-positive U87 cell-derived xenografts and FAP-negative C6-derived xenografts using small-animal T1-weighted 7.0T MR imaging. The longitudinal correlation coefficient (r1) of the agent was 3.813 mM^-1·S^-1. The administration of the Gd-FAPI04 Dimer probe showed a notable enhancement of tumor contrast on T1-weighted whole-body MRI. At 10 and 30 minutes post-injection, the U87 subcutaneous tumor demonstrated significantly greater contrast enhancement than the C6 subcutaneous tumor (P <0.05). In vivo, the safety of the Gd-FAPI-04 Dimer probe was evaluated, which showed no tissue damage in vital organs like the heart, liver, spleen, lung, and kidneys, as indicated by unchanged morphology compared to a normal saline control group. The novel Gd-FAPI04 Dimer molecular probe, Gd-DOTA-Suc-Lys-(FAPI-04)₂ specifically targeting FAP may serve as a safe and promising tool for the diagnostic imaging of solid tumors.

Background: Autism spectrum disorder (ASD) is a highly prevalent neurodevelopmental disorder. However, its diagnosis and effective treatment present challenges. Understanding neurotransmitter impairments may offer new perspectives into the mechanisms underlying ASD and the potential therapeutic targets for this condition. This study aimed to investigate the spatial associations of ASD‐related brain activity patterns and multiple specific neurotransmitter distributions to identify abnormal neurotransmitter alterations in patients with ASD, and to assess how these spatial associations relate to clinical features. Methods: We included 44 patients with ASD and 132 typically developing controls (TDCs) and compared the regional homogeneity (ReHo) differences between the two groups. Associations between the spatial patterns of ReHo alterations and specific neurotransmitter receptor/transporter densities in patients with ASD were evaluated, and the correlations of these associations with the clinical characteristics were analyzed. Results: In comparison with TDCs, patients with ASD exhibited specific brain activity abnormalities in the visuomotor network, cerebro‐cerebellar circuits, angular gyrus, and limbic areas. These atypical brain activity patterns were significantly co‐localized with the serotonergic, glutamatergic, GABAergic, dopaminergic, noradrenergic, cholinergic, and cannabinoid neurotransmitter systems in patients with ASD, and the results showed good reproducibility between different neurotransmitter maps. Additionally, the awareness score in the Social Responsiveness Scale ( ρ = −0.475, p = 0.009) and the social score in the Autism Diagnostic Observation Schedule ( ρ = −0.415, p = 0.049) exhibited negative correlations with the strength of ReHo co‐localization of serotonin 5‐hydroxytryptamine receptor subtype 2a. Conclusions: This is the first systematic analysis of multiple neurotransmitter systems to show abnormalities in these systems in patients with ASD. These results will enhance the existing understanding of the mechanisms underlying ASD and may provide the foundation for identifying therapeutic targets.