Grief is a universal yet multifaceted emotional response to loss, profoundly affecting psychological and biological systems. This review aims to examine the neurobiological mechanisms underlying grief, with a particular focus on prolonged grief disorder, a condition characterized by persistent, maladaptive grief symptoms that extend beyond culturally normative grieving periods. This narrative review synthesizes recent findings on the neurobiology of grief. Hormonal dysregulation, such as elevated oxytocin and cortisol levels, plays a significant role in the physiological response to grief. Epigenetic modifications of stress-related genes further contribute to individual variability in grief responses. Neural alterations are observed in key brain regions associated with memory, emotion regulation, and attachment, including the amygdala, hippocampus, and prefrontal cortex. Dysfunction of the hypothalamic-pituitary-adrenal axis, coupled with disruptions in the default mode network and reward systems, have been implicated in the persistence of pathological grief symptoms. These neurobiological disruptions reflect the interplay among emotional processing, cognitive regulation, and the stress response during grief. By improving our understanding of the biological basis of maladaptive grief responses, these findings provide a foundation for developing targeted therapeutic interventions and guiding future research to better address the needs of individuals experiencing prolonged grief.

Brain aneurysms can be treated with flow diversion embolization. We describe a case of an internal carotid artery aneurysm treated with the Pipeline Vantage flow diverter device, who developed a post-procedural retinal hemorrhage, presenting as an acutely presenting, painless “floater” in the visual field. Outpatient evaluation by a retinal specialist yielded a recommendation to observe the hemorrhage, with the option to intervene with retinal surgery if the hemorrhage worsens or does not resolve. Within one month, there was substantial improvement in his visual symptoms without need for further intervention, and follow-up imaging demonstrated that the aneurysm was successfully treated.

Background: Parkinson’s Disease (PD) is characterized by motor and non-motor symptoms that can overlap with other movement disorders, complicating accurate diagnosis and monitoring. Wearable technologies, such as smartwatches, offer continuous and objective assessment of motor function, but their clinical utility in multiclass classification and symptom prediction remains underexplored. This study aimed to determine whether smartwatch-derived motor features can distinguish idiopathic PD from other movement disorders and whether motor variability is associated with non-motor symptom burden in PD. Methods: We analyzed data from the Parkinson’s Disease Smartwatch (PADS) dataset ( N = 469), which includes accelerometer and gyroscope signals recorded during 20 standardized motor tasks. For each participant, mean and standard deviation values for each axis were averaged across tasks. Diagnostic group classification was assessed using multinomial logistic regression. Among individuals with idiopathic PD ( n = 276), linear regression evaluated associations between motor variability and total non-motor symptom scores from a 30-item questionnaire. Results: Motor variability features, particularly accelerometer Y-axis and gyroscope X-axis standard deviations, significantly differentiated diagnostic groups (pseudo R 2 = 0.068). Age, sex, and handedness also contributed. In the PD subgroup, higher accelerometer X and gyroscope X variability were associated with greater non-motor symptom burden, while greater stability in the mediolateral (Y) axis was linked to fewer symptoms (adjusted R 2 = 0.0081, p < 0.001). Conclusion: Smartwatch-derived motor variability features can modestly differentiate movement disorder diagnoses and are associated with non-motor symptom severity in PD. Our findings support the complementary use of wearable sensors in clinical assessment and remote monitoring. Our findings also lay the foundation for future integration of wearable-derived data into telemedicine workflows.

Brain aneurysms can be treated with flow diversion embolization. We describe a case of an internal carotid artery aneurysm treated with the Pipeline Vantage flow diverter device, who developed a post-procedural retinal hemorrhage, presenting as an acutely- presenting, painless “floater” in the visual field. Outpatient evaluation by a retinal specialist yielded a recommendation to observe the hemorrhage, with the option to intervene with retinal surgery if the hemorrhage worsens or does not resolve. Within one month, there was substantial improvement in his visual symptoms without need for further intervention, and follow-up imaging demonstrated that the aneurysm was successfully treated.

Background: Aluminium-induced neurotoxicity has become a subject of substantial concern because of its consequential effects, including its potential role in neurodegenerative disease pathogenesis. It is thought to occur through multiple mechanisms including the generation of reactive oxygen species and the disruption of cellular homeostasis leading to neuronal damage and dysfunction. However, despite growing evidence of aluminium-induced neurotoxicity, the precise mechanisms underlying its effects and potential therapeutic strategies remain incompletely understood. Its manifestations therefore need to be explored so that its adverse effects can be attenuated. Methods: In the present study, we investigated the neurotoxic effects of aluminium chloride (AlCl 3 ) in relation to neurobehavioural changes and oxidative damage. We also assessed the therapeutic role and protective effects of aqueous extract of Phoenix dactylifera L. fruit (AEPDLF) on antioxidant levels (catalase and superoxide dismutase) and neurobehavioural patterns in adult female Wistar rats. Results: Thirty adult female Wistar rats were divided into five groups (N =30, each group n =6). Control group (A) rats received 2 mL/kg body weight/day (bw/d) of distilled water, and rats in the other four groups (B, C, D, and E) received 200 mg/kg bw/d of AlCl 3 for 28 days. In addition, the treated groups (C, D, and E) received 250, 500, and 1000 mg/kg bw/d, respectively, of AEPDLF for 28 days. On the last day of administration, neurobehavioural assessments were performed. Rats were then sacrificed and brains were harvested and homogenised for biochemical assays. With AlCl 3 treatment, body weight decreased more than brain weight. There was also significantly reduced locomotion with AlCl 3 treatment; however, dose-dependent amelioration was observed with AEPDLF. Although group B had significantly fewer entries into baited arms, and more entries into non-baited arms than group A in the radial arm maze, these changes were ameliorated in groups C, D, and E in an AEPDLF dose-dependent manner. Furthermore, AlCl 3 treatment lowered catalase and superoxide dismutase levels, and these changes were mitigated by AEPDLF in a dose-dependent fashion. Conclusion: The protective capacity of AEPDLF in female rats most efficiently combatted neurotoxicity at 1000 mg/kg bw/d in response to chronic (28 d) AlCl 3 exposure.

Objective: Amyloid-β (Aβ) positron emission tomography (PET) imaging is essential for diagnosing and monitoring Alzheimer’s disease (AD). The Centiloid (CL) scale standardizes Aβ quantification across centers and tracers, but its limitations include calibration requirements and the inability to capture regional A| heterogeneity. Methods: The ComBat-Centiloid method harmonizes A| PET data without calibration by combining a 11C-Pittsburgh Compound B standard reference database with the ComBat algorithm and CL framework to generate harmonized CL (HCL) and harmonized regional CL (HRCL) values. Pearson correlation analysis was used to evaluate the relationship between HCL and CL values within the same tracer/protocol combinations. Paired t -tests were used to assess differences in HCL and CL values between two same-subject scans using different tracers taken within 1 year. Multicenter analyses were performed with combined datasets with different tracer/protocols to compare the consistency of HRCL, regional CL (RCL), and SUVR for differentiating patients with AD from cognitively normal (CN) individuals. Results: HCL values strongly correlated with CL across all tracer/protocol combinations and effectively eliminated inter-tracer biases, showing no significant differences in paired tests. In multicenter analyses, HCL values outperformed SUVR and RCL, demonstrating superior consistency for distinguishing patients with AD from CN individuals. Conclusion: The ComBat-Centiloid method eliminates calibration requirements and supports robust harmonized assessments in multicenter multitracer studies.

Schizophrenia includes positive, negative, and cognitive symptoms. Negative and cognitive symptoms do not benefit from current treatments and currently are the main determinants of functional outcome. In the European Union, where healthcare is widely accessible, 80%-90% of patients with schizophrenia are unemployed, while 10% of them die by suicide. Currently, it is believed that psychosis and schizophrenia’s positive symptoms stem from excessive dopamine D2 activity in the striatum, leading to ‘hyper-salience’ followed by delusions, and in the sensory cortex leading to ‘self-generated sensory activity’ followed by hallucinations. The reviewed evidence in this article suggests open potassium and hyperpolarization-activated cyclic nucleotide-gated (HCN) channels leading to prefrontal cortex (PFC) dysfunction followed by ‘cognitive impairment’/’loss of insight’/’lack of deliberate reasoning’/’lack of reality monitoring’ to also be a contributing factor in psychosis and schizophrenia. This could explain how kappa-opioid agonists and potassium channel openers induce psychosis while lowering dopamine but opening potassium channels; how nicotine improves certain schizophrenia symptoms while increasing dopamine but closing potassium/HCN channels; how insightfulness is maintained with 5HT2A psychedelics which increase dopamine but close potassium channels; why guanfacine which closes potassium/HCN channels is the best treatment in delirium psychosis which is characterized by prominent cognitive dysfunction; and why clozapine which closes potassium/HCN channels is superior to other antipsychotics. This article concludes that having a cognitive deficit in the first place may make someone more susceptible to developing all schizophrenia symptoms and that potassium/HCN channel blockers would improve that. They would especially ameliorate the neglected cognitive and negative symptoms. This article also notes the importance of norepinephrine and NMDA. Lastly, it proposes treatment perspectives, summarizes the reviewed findings in Table 1, and presents theorized pathways behind schizophrenia and psychosis in Figure 1.

Movement disorder management and therapy are rapidly evolving, owing to an ever-deeper understanding of disease biology and the discovery of new tools for diagnosis and treatment. With this narrative review, we aim to explore emerging therapeutic approaches for movement disorders, with a focus on Parkinson’s disease (PD) and other movement-related pathological conditions, including Huntington’s disease (HD), essential tremor (ET), and dystonia. This review encompasses preclinical research and human trials, providing a comprehensive overview of the current landscape. Several promising therapeutic strategies have emerged, particularly in the realm of precision medicine for PD associated with GBA and LRRK2 gene mutations. Additionally, innovative immunotherapies and drugs targeting misfolded α-synuclein are under investigation. These approaches have the potential to influence disease progression and improve patient outcomes. The landscape of pharmacological treatments for movement disorders is both complex and diverse, with substantial progress made over the years. While current treatments effectively manage motor symptoms, they fall short of providing a definitive cure and are limited by nonmotor symptoms and potential side effects. Novel techniques, such as gene therapy, stem cell therapy, and infusion therapies, offer promising avenues for future research.

Alzheimer’s disease (AD) is a critical issue that affects both the quality of life of families and public health. Despite years of research, single-target therapies for AD remain limited. This is primarily because of the complex and multifaceted pathological mechanisms underlying AD. Recent findings of the involvement of gut microbiome dysbiosis in AD pathogenesis have offered novel insights, emphasizing the need for holistic approaches. As AD progresses, gut microbiota alterations contribute to metabolic and immune imbalances, sparking peripheral inflammation. Consequently, there is heightened infiltration of immune cells into the brain, thus exacerbating neuroinflammation and cognitive decline. Notably, drug developments targeting this mechanism have witnessed substantial advancements, presenting novel systematic treatment approaches for AD patients. Furthermore, the gut microbiota plays a pivotal role in many other diseases and their associated cognitive impairments. The gut-brain axis, a bidirectional communication network, therefore holds significant promise for AD treatment as well as broader cognitive impairment solutions, beyond those based on the amyloid-beta and tau theories.

Driven by the development of evidence-based medicine, cohort studies provide reliable and scientific evidence for brain health and neurological disorders. This review provides a concise introduction to several internationally renowned classical cohorts, highlighting their notable contributions to brain health research. Additionally, it provides a brief introduction to disease-specific cohorts in the field of brain science along with their research outcomes. Moreover, the review examines Chinese cohorts related to brain health and discusses the significant findings from the related studies. Increased interdisciplinary cooperation and cohort data sharing are expected to generate new ideas and scientific standards for the early diagnosis of neurological diseases and personalized prevention and treatment strategies in the future, thereby effectively improving brain health.