Schizophrenia (SCZ) is a chronic mental disorder that typically starts in early adulthood. It is characterised by structural brain abnormalities that occur early in the course of the disease, such as changes in the synapses and alterations in the brain white matter, which consequently progress to brain atrophy in several regions of the brain, as well as white matter lesions. On the other hand, epidemiological evidence indicates improved survival and increased life expectancy among patients with SCZ, largely due to advances in diagnosis and medication management, resulting in a growing number of individuals reaching older age. In addition, several studies have shown accelerated aging and an increased risk of cognitive decline in these patients. Consequently, the healthcare system faces a growing challenge: older adults with chronic SCZ who are at increased risk of dementia (particularly Alzheimer-type dementia). Notably, many individuals with chronic SCZ have several modifiable risk factors for dementia, including obesity, diabetes, elevated low-density lipoprotein cholesterol (LDL), metabolic syndrome, physical inactivity, smoking, and social isolation which may result from a combination of long-term antipsychotic medication, lifestyle factors, and medical comorbidities. These factors overlap substantially with established risk factors for Alzheimer’s disease (AD) and may contribute to increased vulnerability to cognitive decline and dementia in later life. The clinical presentation of older adults with chronic SCZ who develop progressive cognitive and functional decline may closely resemble AD, owing to overlapping features such as memory impairment, social withdrawal, psychomotor slowing, and gait disturbances associated with vascular and metabolic comorbidities. Distinguishing these conditions represents a major diagnostic challenge for cognitive neurologists and psychogeriatricians. Therefore, this narrative review critically examines the differential and overlapping neuroimaging features of chronic SCZ and AD to facilitate more accurate clinical assessment and diagnosis in late life.

The global prevalence of Autism Spectrum Condition (ASC) is increasing, yet effective supportive interventions remain largely unidentified, highlighting the urgent need to clarify the underlying neuropathophysiology. Neuroimaging offers a pathway toward this understanding; however, most studies rely on indirect measures of neurophysiology, whereas direct approaches such as [18F]Fluorodeoxyglucose positron emission tomography (FDG-PET) remain underutilized and lack systematic synthesis in the literature. This review and meta-analysis evaluated FDG-PET research in ASC. A systematic search identified 2,725 records, of which 21 studies compared FDG-PET findings between autistic and neurotypical individuals. Nine met the inclusion criteria for the review, and eight were included in the meta-analysis. The review revealed inconsistent findings, reporting both increased and decreased glucose metabolism in ASC, likely reflecting methodological heterogeneity. The meta-analysis found no statistically significant differences, but indicated a weak non-significant trend toward elevated glucose metabolism in the striatum in autistic compared to neurotypicals individuals (standardized mean difference [SMD] = 0.416; 95

Differentiating Alzheimer's disease (AD) from frontotemporal dementia (FTD) remains a major clinical challenge, particularly in early disease stages when phenotypic overlap is common and in later stages when cortical degeneration becomes widespread. Structural magnetic resonance imaging (MRI) provides a widely available, non-invasive framework for assessing region-specific brain atrophy patterns associated with these disorders. This narrative review synthesizes current evidence on MRI-based approaches for distinguishing FTD from AD across disease stages. FTD, particularly the behavioral variant, is characterized by early and prominent degeneration of frontal and anterior temporal networks, frequently with hemispheric asymmetry and early behavioral change, including apathy as a core feature. In contrast, AD typically demonstrates a posterior-predominant pattern, with medial temporal and temporoparietal atrophy reflecting a posterior-to-anterior trajectory, while frontal involvement emerges later except in atypical variants. Quantitative MRI techniques, including voxel-based morphometry, cortical thickness analysis, and asymmetry indices, together with validated visual rating scales, enhance the detection of these spatial patterns. Fluid-attenuated inversion recovery imaging supports interpretation by identifying vascular burden, and complementary biomarkers, including FDG-PET, cerebrospinal fluid, and blood-based markers, provide molecular and functional context in diagnostically ambiguous cases. The diagnostic specificity of frontal atrophy is greatest in early stages and decreases as AD and FTD converge anatomically in moderate to advanced disease. Accurate differential diagnosis, therefore, requires a stage-aware, integrative framework that combines structural MRI with longitudinal clinical assessment, neuropsychological profiling, and biomarker information. Structural MRI remains the cornerstone of differentiation, with regional atrophy patterns interpreted within a broader clinical and biological context rather than in isolation.

The glymphatic system supports brain homeostasis by clearing interstitial solutes via perivascular pathways. Alterations in glymphatic function have been linked to neurodevelopmental and neurodegenerative disorders, but its role in autism spectrum disorder (ASD) remains unclear. We analyzed diffusion tensor imaging (DTI) magnetic resonance imaging data from five cohorts in the Autism Brain Imaging Data Exchange (ABIDE) project. Glymphatic function was estimated using the DTI analysis along the perivascular space (ALPS) index. ASD diagnoses were confirmed according to DSM-IV-TR or DSM-5 criteria, and neurotypical (NT) participants had no history of neurological, psychiatric, or developmental disorders. The final sample comprised 250 participants (128 ASD, mean age = 18.57 ± 13.81; 122 NT, mean age = 21.32 ± 14.37). Two-way analysis of variance (ANOVA) revealed a significant main effect of diagnosis, F(1, 246) = 10.44, p = 0.0014, with lower ALPS-indices in ASD. A diagnosis-by-age interaction was also observed, F(1, 246) = 4.71, p = 0.031. Post hoc tests demonstrated that autistic adults (≥ 18 years) had significantly lower ALPS-indices than NT adults (p = 0.0004), whereas no group differences were demonstrated between younger ASD and NT (< 18 years). In ASD adults, the ALPS-index correlated negatively with depressive symptoms (r = − 0.489, p = 0.013), but not with IQ or autistic traits. These findings suggest that glymphatic dysfunction in ASD may follow a developmental trajectory, with alterations becoming most evident in adulthood, potentially contributing to an increased risk of developing neurodegenerative disorder in autistic individuals.

Dopaminergic signalling and glucose metabolism have been implicated in autism spectrum disorder (ASD), yet in vivo evidence in the human brain remains largely unexplored. This study examined subcortical dopamine D2 receptor availability and glucose metabolism in ASD to assess their clinical relevance. In this dual-tracer PET/MR case–control study, 30 autistic and 30 neurotypical adults (age-, sex-, body mass index-, and IQ-matched) underwent [11C]raclopride PET to assess dopamine D2 receptor availability, [1⁸F]FDG PET to measure glucose metabolism and resting-state fMRI to evaluate functional connectivity. Autistic individuals demonstrated increased D2 receptor availability in the thalamus, with additional increases in the nucleus accumbens and putamen among autistic males compared to neurotypical males. Glucose metabolism was elevated in the thalamus and globus pallidus in ASD relative to NT, and this pattern persisted within both autistic males and autistic females in sex‑stratified comparisons. Globus pallidus and thalamic glucose metabolism correlated positively with social and communication difficulties. Resting-state fMRI analyses revealed diagnosis- and sex-dependent correlations between thalamic D2 receptor availability and functional connectivity. This study provides in vivo evidence of elevated subcortical D2R availability and glucose metabolism in autistic adults, a pattern observed across sexes. We also show that D2R availability is tightly linked to glucose metabolism and that D2R-functional connectivity coupling is altered in ASD, both relative to neurotypical adults and between autistic males and females. These findings highlight dopaminergic mechanisms as potential biomarkers and therapeutic targets in ASD.

Alzheimer's disease (AD) affects the hippocampus early and profoundly, yet its complex three-dimensional (3D) anatomy can be difficult to appreciate on conventional imaging. Recognizing hippocampal atrophy in amnestic mild cognitive impairment (MCI) is essential for timely diagnosis and clinical decision-making. This study aimed to create a tangible 3D hippocampal model derived from magnetic resonance imaging (MRI) to support neuroeducation, enhance clinician training, and improve visualization of disease-related change. High-resolution T1-weighted MRI scans were obtained from 9 cognitively healthy controls (HC), 10 individuals with MCI, and 10 with AD. Semi-automated segmentation was used to reconstruct 3D hippocampal models for each group. Volumetric analyses assessed hippocampal atrophy, hemispheric asymmetry, and diagnostic differentiation. The hemisphere showing the most pronounced atrophy was selected for physical modeling, and an experienced neurologist reviewed a 3D-printed hippocampus for anatomical accuracy and educational value. Significant volumetric differences were identified in both hippocampal hemispheres across HC, MCI, and AD (p < .001). The right hippocampus demonstrated the greatest atrophy in AD and early volume loss in MCI. Receiver operating characteristic analysis showed strong diagnostic performance, with areas under the curve of 0.980 for AD versus MCI and 0.833 for MCI versus HC. Based on these findings, the right hippocampus was selected for 3D printing. MRI-derived 3D-printed hippocampal models translate complex neuroimaging data into accessible, tactile representations of AD-related degeneration. This approach has potential value for medical education, clinician training, patient-clinician communication, and public awareness, as it makes hippocampal atrophy more clearly visible and understandable.

Dementia is a progressive and ultimately life-limiting condition that represents a major cause of disability worldwide. Alzheimer’s disease (AD) is the most prevalent form of dementia that constitutes approximately 60–70

Despite growing awareness, diagnosing Autism Spectrum Condition (ASC) in adulthood remains challenging due to a limited range of diagnostic tools beyond psychological assessments. Although recent neuroimaging advancements have identified social brain regions (SBR) associated with sociability, research on these areas in ASC, particularly within the largely understudied adult ASC population, remains scarce. Explore functional and volumetric differences in the SBR between autistic and neurotypical individuals. We conducted a volumetric and functional assessment of SBRs using open-source MRI data from the Autism Brain Imaging Data Exchange (ABIDE). The sample included 44 adult ASC (37 male, mean age 25.86 ± 6.58) and 64 adult neurotypical individuals (51 male, mean age 25.36 ± 4.05). Autistic adult individuals demonstrated lower left nucleus accumbens volume. The amplitude of low frequency fluctuations was enhanced in the orbitofrontal cortex and temporoparietal junction, and decreased in the caudate, hippocampus, thalamus, and ventral tegmental area in the autistic group. Additionally, a widespread increase in functional connectivity within the SBR was demonstrated in the ASC group. Structural and functional measures allowed classification of autistic and neurotypical individuals with 76% accuracy using a support vector machine model. The results demonstrate significant SBR differences between adult autistic and neurotypical individuals, highlighting the SBR as potentially essential in ASC etiology, we demonstrate its ability to classify autistic and neurotypical individuals. However, further exploration of the SBR using advanced imaging techniques is required.

The purpose of this study was to advance our understanding of the neurobiology of healthy aging, which is crucial for improving quality of life and preventing age-related diseases. Despite its importance, a comprehensive investigation of this process has yet to be fully characterized. We used a hybrid PET/MRI scanner to assess neurophysiological parameters in 80 healthy individuals aged 20–78. Cerebral amyloid-beta (Aβ) deposition and glucose metabolism were assessed using PET scans, while participants underwent simultaneous MRI scans. We found a positive correlation between Aβ-deposition and aging, and a negative correlation between glucose metabolism and aging. The insula showed the strongest negative correlation between glucose metabolism and age (Spearman’s r = -0.683, 95

Since Cajal introduced dendritic spines in the 19th century, they have attained considerable attention, especially in neuropsychiatric and neurologic disorders. Multiple roles of dendritic spine malfunction and pathology in the progression of various diseases have been reported. Thus, it is inevitable to consider these structures as new therapeutic targets for treating neuropsychiatric and neurologic disorders such as autism spectrum disorders, schizophrenia, dementia, Down syndrome, etc. Therefore, we attempted to prepare a narrative review of the literature regarding the role of dendritic spines in the pathogenesis of aforementioned diseases and to shed new light on their pathophysiology.

Background. This study assessed the potential efficacy of donepezil in treating autism spectrum disorder (ASD), a neurodevelopmental condition characterized by social communication difficulties and repetitive behaviors. Donepezil, primarily used to treat Alzheimer’s disease as an acetylcholinesterase inhibitor, has gained attention as a potential treatment for ASD symptoms. Methods. Following PRISMA guidelines, a systematic review was conducted to investigate the effects of donepezil on individuals with ASD. Outcome measures assessed various aspects of ASD, including language skills, executive function, behavior, and core symptoms. Nine studies were identified, including four randomized controlled trials (RCTs), three retrospective studies, one open-label trial, and one case report. Results. One RCT reported significant improvements in expressive and receptive language skills, especially in younger children. Another study combining donepezil with choline supplementation showed enhanced receptive language skills, particularly in younger participants. An open-label trial indicated improved rapid eye movement sleep patterns in autistic children treated with donepezil. Several retrospective studies reported improvements in behavioral symptoms, such as aggression and hyperactivity. However, other RCTs did not find statistically significant improvements in executive functioning. Conclusion. In general, donepezil use in ASD demonstrates promise in specific areas, notably language development and behavioral symptom management. However, the results are contradictory, requiring further research to clarify its role, optimal dosing, long-term effects, and potential side effects in individuals with ASD. Practical Implications. Donepezil can be used to improve the clinical global impression and language skills of people with ASD.

Abstract Background  An accurate monitoring technique is crucial in brain tumors to choose the best treatment approach after surgery and/or chemoradiation. Radiological assessment of brain tumors is widely based on the magnetic resonance imaging (MRI) modality in this regard; however, MRI criteria are unable to precisely differentiate tumoral tissue from treatment-related changes. This study was conducted to evaluate whether fused MRI and O-(2- 18 F-fluoroethyl)-L-tyrosine ( 18 F-FET) positron emission tomography (PET) can improve the diagnostic accuracy of the practitioners to discriminate treatment-related changes from true recurrence of brain tumor. Methods  We retrospectively analyzed 18 F-FET PET/computed tomography (CT) of 11 patients with histopathologically proven brain tumors that were suspicious for recurrence changes after 3 to 4 months of surgery. All the patients underwent MRI and 18 F-FET PET/CT. As a third assessment, fused 18 F-FET PET/MRI was also acquired. Finally, the diagnostic accuracy of the applied modalities was compared. Results  Eleven patients aged 27 to 73 years with a mean age of 47 ± 13 years were enrolled. According to the results, 9/11 cases (82%) showed positive MRI and 6 cases (55%) showed positive PET/CT and PET/MRI. Tumoral recurrence was observed in six patients (55%) in the follow-up period. Based on the follow-up results, accuracy, sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) were 64, 85, 25, 67, and 50%, respectively, for MRI alone and 91, 85, 100, 100, and 80%, respectively, for both PET/CT and PET/MRI. Conclusion  This study found that 18 F-FET PET-MR image fusion in the management of brain tumors might improve recurrence detection; however, further well-designed studies are needed to verify these preliminary data.

Cognition and brain homeostasis depends on cerebral blood flow to secure adequate oxygen and nutrient distribution to the brain tissue. Altered cerebral blood flow has previously been reported in individuals diagnosed with autism spectrum condition in comparison to non-autistics. This phenomenon might suggest cerebral blood flow as a potential biomarker for autism spectrum condition. Major technological advancement enables the non-invasive and quantitative measurement of cerebral blood flow via arterial spin labeling magnetic resonance imaging. However, most neuroimaging studies in autistic individuals exploit the indirect blood oxygen level dependent functional magnetic resonance imaging signal instead. Therefore, this review examines the use of arterial spin labeling to further investigate the neurobiology of the autism spectrum condition. Followed by a comparison of results from molecular imaging and arterial spin labeling studies and a discussion concerning the future direction and potential of arterial spin labeling in this context. We found that arterial spin labeling study results are consistent with those of molecular imaging, especially after considering the effect of age and sex. Arterial spin labeling has numerous application possibilities besides the quantification of cerebral blood flow, including assessment of functional connectivity and arterial transit time. Therefore, we encourage researchers to explore and consider the application of arterial spin labeling for future scientific studies in the quest to better understand the neurobiology of autism spectrum condition. Lay abstract Brain function and health depend on cerebral blood flow to secure the necessary delivery of oxygen and nutrients to the brain tissue. However, cerebral blood flow appears to be altered in autistic compared to non-autistic individuals, potentially suggesting this difference to be a cause and potential identification point of autism. Recent technological development enables precise and non-invasive measurement of cerebral blood flow via the magnetic resonance imaging method referred to as arterial spin labeling. However, most neuroimaging studies still prefer using the physiologically indirect measure derived from functional magnetic resonance imaging. Therefore, this review examines the use of arterial spin labeling to further investigate the neurobiology of autism. Furthermore, the review includes a comparison of results from molecular imaging and arterial spin labeling followed by a discussion concerning the future direction and potential of arterial spin labeling. We found that arterial spin labeling study results are consistent with those of molecular imaging, especially after considering the effect of age and sex. In addition, arterial spin labeling has numerous application possibilities besides the quantification of cerebral blood flow. Therefore, we encourage researchers to explore and consider the application of arterial spin labeling for future scientific studies in the quest to better understand the neurobiology of autism.

We derived three widely used linearizations from the definition of receptor availability in molecular imaging with positron emission tomography (PET). The purpose of the present research was to determine the convergence of the results of the 3 methods in terms of 3 parameters-occupancy (s), distribution volume of the nondisplaceable reference binding compartment (VND), and nondisplaceable reference binding potential (BPND) of the radioligand-in the absence of a gold standard. We tested 104 cases culled from the literature and calculated the goodness of fit of the least-squares and Deming II methods of linear regression when applied to the determination of s, VND, and BPND using the goodness-of-fit parameters R2, coefficient of variation (root-mean-square error [RMSE]), and the infinity norm (‖X‖∞) with both regression methods. We observed superior convergence among the values of s, VND, and BPND for the inhibition and occupancy plots. The inhibition plot emerged as the plot with a slightly higher degree of convergence (based on R2, RMSE, and ‖X‖∞ value). With two regression methods (the least-squares method [LSM] and the Deming II [DM] method), the estimated values of s, VND, and BPND generally converged. The inhibition and occupancy plots yielded the best fits to the data, according to the goodness-of-fit parameters, due primarily to absence of commingling of the dependent and independent variables tested with the saturation (original Lassen) plot. In the presence of noise, the inhibition and occupancy plots yielded higher convergences.

The present study aims to evaluate the combined effect of ischaemic postconditioning (IPostC) and nicotinamide mononucleotide (NMN) on cardioprotection and mitochondrial function in aged rats subjected to myocardial ischaemia–reperfusion (IR) injury. Sixty aged Wistar rats were randomly divided into five groups (n = 12), including sham, control, NMN, IPostC, and NMN + IPostC. Regional ischaemia was induced by 30‐min occlusion of the left anterior descending coronary artery (LAD) followed by 60‐min reperfusion. IPostC was applied at the onset of reperfusion, by six cycles of 10‐s reperfusion/ischaemia. NMN (100 mg/kg) was intraperitoneally injected every other day for 28 days before IR. Myocardial haemodynamics and infarct size (IS) were measured, and the left ventricles samples were harvested to assess cardiac mitochondrial function. The results showed that all treatments reduced lactate dehydrogenase release compared to those of the control group. IPostC alone failed to reduce IS and myocardial function. However, NMN and combined therapy could significantly improve myocardial function and decrease the IS compared to the control animals. Moreover, the effects of combined therapy on the decrease of IS, mitochondrial reactive oxygen species (ROS), and improvement of mitochondrial membrane potential (MMP) were greater than those of stand‐alone treatments. These results demonstrated that cardioprotection by combined therapy with NMN + IPostC was superior to individual treatments, and pretreatment of aged rats with NMN was able to correct the failure of IPostC in protecting the hearts of aged rats against IR injury.

Spinal cord injury (SCI) can result in significant neurological impairment and functional and cognitive deficits. It is well established that SCI results in focal neurodegeneration that gradually spreads to other cord areas. On the other hand, traumatic brain injury (TBI) is strongly associated with tau protein pathology and neurodegeneration that can spread in areas throughout the brain. Tau is a microtubule-associated protein abundant in neurons and whose abnormalities result in neuronal cell death. While SCI and TBI have been extensively studied, there is limited research on the relationship between SCI and brain tau pathology. As a result, in this study, we examined tau pathology in spinal cord and brain samples obtained from severe SCI mouse models at various time points. The effects of severe SCI on locomotor function, spatial memory, anxiety/risk-taking behavior were investigated. Immunostaining and immunoblotting confirmed a progressive increase in tau pathology in the spinal cord and brain areas. Moreover, we used electron microscopy to examine brain samples and observed disrupted mitochondria and microtubule structure following SCI. SCI resulted in motor dysfunction, memory impairment, and abnormal risk-taking behavior. Notably, eliminating pathogenic cis P-tau via systemic administration of appropriate monoclonal antibodies restored SCI’s pathological and functional consequences. Thus, our findings suggest that SCI causes severe tauopathy that spreads to brain areas, indicating brain dysfunction. Additionally, tau immunotherapy with an anti-cis P-tau antibody could suppress pathogenic outcomes in SCI mouse models, with significant clinical implications for SCI patients. SCI induces profound pathogenic cis p-tau, which diffuses into the brain through CSF, resulting in brain neurodegeneration and cognitive decline.

Ischaemic heart diseases are one of the major causes of death in the world. In most patients, ischaemic heart disease is coincident with other risk factors such as diabetes. Patients with diabetes are more prone to cardiac ischaemic dysfunctions including ischaemia-reperfusion injury. Ischaemic preconditioning, postconditioning and remote conditionings are reliable interventions to protect the myocardium against ischaemia-reperfusion injuries through activating various signaling pathways and intracellular mediators. Diabetes can disrupt the intracellular signaling cascades involved in these myocardial protections, and studies have revealed that cardioprotective effects of the conditioning interventions are diminished in the diabetic condition. The complex pathophysiology and poor prognosis of ischaemic heart disease among people with diabetes necessitate the investigation of the interaction of diabetes with ischaemia-reperfusion injury and cardioprotective mechanisms. Reducing the outcomes of ischaemia-reperfusion injury using targeted strategies would be particularly helpful in this population. In this study, we review the protective interventional signaling pathways and mediators which are activated by ischaemic conditioning strategies in healthy and diabetic myocardium with ischaemia-reperfusion injury.