Traumatic brain injury (TBI) is a leading cause of neurological dysfunction worldwide, often resulting in long-lasting cognitive, motor, and psychiatric disorders. This review presents a comprehensive analysis of the neurological complications that arise following TBI, focusing on the underlying mechanisms and the clinical manifestations observed in affected patients. TBI induces a complex cascade of biochemical events, including neuronal injury, neuroinflammation, oxidative stress, and excitotoxicity, which collectively contribute to the onset of various neurological disorders. One of the most common and debilitating consequences of TBI is post-traumatic epilepsy (PTE), which frequently develops in patients as a long-term sequela. The review discusses the pathophysiology of PTE, examining how brain injury alters neuronal excitability and predisposes patients to recurrent seizures. In addition to epilepsy, TBI often leads to cognitive impairments, such as memory loss, attention deficits, and executive dysfunction, which significantly affect patients’ daily functioning. Motor impairments, including weakness, spasticity, and coordination issues, are common among TBI patients and can severely limit their mobility and independence. These motor deficits are primarily associated with injury to the motor cortex, basal ganglia, and cerebellum. Psychiatric disorders, such as depression, anxiety, and post-traumatic stress disorder, are prevalent in TBI patients and further complicate their recovery. This review emphasizes the need for early diagnosis, targeted interventions, and novel therapeutic strategies to manage the diverse and complex neurological consequences of TBI. A deeper understanding of the pathophysiology and clinical manifestations of TBI-related neurological disorders is crucial for improving patient outcomes and enhancing quality of life.

Alzheimer’s disease (AD) is the most common cause of age-related dementia and death, resulting from the aggregation of tau protein into insoluble neurofibrillary tangles (NFTs) composed of paired helical filaments and straight filaments. Graphene quantum dots (GQDs), a unique form of nanoparticles, have emerged as a crucial tool for the detection and diagnosis of AD. They are considered attractive due to their fluorescence-emitting capabilities, nanoscale size, chemical stability, solubility, and ease of synthesis. In this review, we investigated the potential of GQDs as a therapeutic tool in AD intervention, highlighting their recent developments, challenges, and future directions. A comprehensive and systematic search was conducted across electronic databases (Scopus, PubMed, Google Scholar, and Medline) for recent and up-to-date articles related to the keywords: “Alzheimer’s disease,” “graphene quantum dots,” “nanoparticles,” and “neuroscience.” Our findings indicate that QDs possess the ability to cross the blood-brain barrier, reduce disease symptoms, and facilitate drug delivery, cell labeling, and neuronal regeneration. In addition, early identification, prevention, and disassembly of tau protein aggregation in AD can be achieved using GQDs. In conclusion, the application of GQDs to improve the progression of AD neuropathology by disintegrating NFTs of tau protein presents a promising approach for diagnostic research in AD. The limitations of GQDs, particularly their long-term exposure to the brain, need to be thoroughly investigated. This includes minimizing the side effects through a multidisciplinary translational neuroscience approach for therapeutic applications in clinical trials.

Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterized by the selective degeneration of nigrostriatal dopaminergic neurons and pathological accumulation of α-synuclein (α-Syn) aggregates. Emerging evidence indicates the important role of lipid metabolism dysregulation in driving these pathological features. As major structural components of brain tissue and critical regulators of neuronal function, lipids are involved in diverse biological processes, including cell membrane formation, intercellular signaling, energy storage, and homeostasis. Their dysregulation directly affects neural functions, such as synaptic transmission, antioxidant defense, and inflammatory modulation. PD is recognized not only as a “proteinopathy” but also as an “organelle communication disorder,” involving dysfunction of membrane contact sites across mitochondria, endoplasmic reticulum, lysosomes, and lipid droplets (LDs)—a process that may constitute an early pathogenic event. It is noteworthy that several proteins mediating LDs-organelle contacts are disease-related factors encoded by mutated genes in inherited neurological and metabolic disorders. Despite the extensive communication between intracellular LDs and other organelles through these contact sites, the systematic integration of lipid metabolism dysregulation into core PD pathogenesis remains elusive. This review provides a comprehensive overview of the mechanisms underlying lipid-organelle interactions in PD pathogenesis, with a specific focus on the triangular interplay among the three core pathological hallmarks: α-Syn aggregation, mitochondrial dysfunction, and neuroinflammation, and their convergence with the lipid metabolic network. By analyzing molecular mechanisms and clinical implications, with particular focus on lipid-related biomarkers and therapeutic strategies targeting organelle communication pathways, this review aims to provide new insights into the role of lipid dyshomeostasis in PD pathogenesis and identify feasible therapeutic targets.

Cerebral small vessel disease (CSVD) is one of the most common vascular diseases of the brain, primarily diagnosed using magnetic resonance imaging biomarkers. Advanced brain imaging techniques have enabled the detection of asymptomatic or covert CSVD in individuals without neurological symptoms. CSVD is highly prevalent among the elderly and healthy community-dwelling adults with vascular risk factors. It increases the risk of stroke, cognitive decline, and vascular dementia, and exacerbates the severity of Alzheimer’s disease. Covert CSVD is generally considered incidental, leading to a lack of intervention, especially among non-neurological physicians. The relevance of CSVD in asymptomatic healthy populations remains a contentious issue. Despite identifying covert CSVD, management strategies are poorly established, posing challenges for neurologists and primary care physicians. Key debated issues are: (i) the advantages of screening asymptomatic individuals concerning reduced adverse health events or cost-effectiveness, (ii) effective community screening strategies, including the development of non-imaging biomarkers, and (iii) the clinical and therapeutic implications of covert CSVD. Currently, limited scientific evidence addresses these issues, necessitating more high-quality longitudinal studies. Increased awareness regarding the importance of detecting, treating, and systematically monitoring covert CVDS is essential. Screening procedures should be more active, utilizing more accessible non-imaging biomarkers such as blood tests, retinal assessments, and ambulatory blood pressure monitoring. The early detection of CSVD presents an opportunity to implement more effective preventive strategies.

Seizure precipitants, which precede the onset of an epileptic seizure, are considered responsible for an epileptic attack. The ultimate goal of treating patients with epilepsy (PWE) is to maintain a seizure-free state with the appropriate treatment. Despite the anti-epileptic treatment, some patients may continue to experience seizures. This study aimed to study the seizure-provoking factors to generate evidence-based information for better management of patients. A facility-based cross-sectional study was conducted at two major referral hospitals with large patient flow in Addis Ababa, Ethiopia, from October 2018 to September 2019. PWEs who had been receiving anti-epileptic treatment before the study were consecutively enrolled until the desired sample size was reached using a convenient sampling technique. A total of 184 PWEs were enrolled. The prevalence of precipitating factors among epilepsy patients was 94%. The most commonly reported precipitating factors were stress (70.1%), missing anti-epileptic dose (57.1%), and inadequate sleep (32.1%). Our findings unveiled factors that precipitate seizures in PWEs and demonstrated the potential of avoiding these factors to reduce the incidence of seizures. It is therefore essential to increase patients’ awareness to focus on non-pharmacological therapy in addition to their regular treatment for better management.

Sleep quality significantly affects cognitive capacities, metabolic functions, and overall well-being in young adult males. However, most studies on sleep disruption in this population rely on self-reported surveys rather than objective assessments, limiting understanding of actual sleep architecture. This cross-sectional comparative study aimed to examine polysomnographic sleep characteristics of young adult males with poor subjective sleep quality compared to established normative values of healthy groups. Sleep quality was assessed using the Pittsburgh sleep quality index, and polysomnography (PSG) was conducted in a controlled laboratory environment. Comprehensive sleep parameters analyzed included total sleep time (TST), sleep efficiency (SE), sleep onset latency (SOL), rapid eye movement (REM) onset latency (ROL), wakefulness (WK), and sleep stages N1, N2, N3, and REM sleep. Independent t-tests were used for PSG data comparison. The study found that young adult males with poor subjective sleep quality had significantly lower TST (t = −7.04, p<0.001), WK (t = −2.721, p=0.01), N2 (t = −5.993, p<0.001), and REM sleep (t = −21.532, p<0.001). Conversely, SE (t = 19.50, p<0.001), SOL (t = 4.75, p<0.001), ROL (t = 3.61, p=0.001), N1 (t = 18.98, p<0.001), and N3 (t = 11.119, p<0.001) were significantly higher. These findings indicate that young adult males with poor subjective sleep quality exhibited significantly different architecture. Notably, their high SE despite perceived poor sleep highlights a discrepancy between subjective perception and objective sleep metrics.

Spinal cord injury (SCI) induces a prolonged and complex inflammatory response that contributes to secondary damage and influences functional recovery. Targeting this inflammatory milieu represents a promising therapeutic strategy. In this study, we investigated the effects of extracellular vesicles (EVs) derived from mesenchymal stem cells (MSCs) and encapsulated in a fibrin matrix (FM) on cytokine regulation in a rat model of SCI 60 days post-injury. MSCs were isolated from rat adipose tissue, and EVs were obtained using cytochalasin B-induced vesiculation. The EVs were encapsulated in FM and applied locally to the injury site at doses of 5 and 10 μg. The SCI rat models were divided into four groups: untreated, treated with FM alone, treated with 5 μg of EVs in FM (FM+EVs5), and treated with a 10 μg dose (FM+EVs10). A multiplex assay was employed to quantify the levels of 23 cytokines in spinal cord tissue homogenates. The application of FM alone altered cytokine levels, notably increasing granulocyte colony-stimulating factor (G-CSF) levels by 2.8-fold, which may be attributed to the hemostatic and bioactive properties of fibrin. Treatment with MSC-derived EVs resulted in a dose-dependent modulation of inflammatory responses. In the FM+EVs10 group, pro-inflammatory cytokines interleukin (IL)-1β and IL-5, as well as the anti-inflammatory cytokine IL-10, were significantly reduced compared to both the untreated and FM-alone groups, with IL-10 levels decreasing 2.4-fold. A similar trend was observed for IL-17A, which was 1.6-fold lower in the FM+EVs10 group compared to the FM-alone group. These findings suggest that fibrin-encapsulated MSC-derived EVs can modulate inflammation in chronic SCI and warrant further investigation as a therapeutic approach for neuroprotection and tissue repair.

The limited availability of medical imaging datasets and concerns over patient privacy pose significant challenges in artificial intelligence-driven disease diagnosis. To overcome these limitations, this study introduces the use of the denoising diffusion model (DDM) for generating synthetic datasets, marking a significant advancement over traditional generative adversarial networks (GANs). This research pioneers the integration of DDM with conditional deep convolutional neural networks (CDCNN) for brain tumor classification, focusing on four categories: Glioma, meningioma, pituitary tumors, and healthy tissue. The proposed CDCNN model, developed from existing convolutional neural network architectures, effectively processed both DDM-generated synthetic datasets and original datasets sourced from the Kaggle repository. The results demonstrate the remarkable efficacy of the DDM-based augmentation framework, with the CDCNN model achieving an accuracy of 96.2%, significantly outperforming traditional GAN-based models, such as Pix2Pix. A comparative analysis against established architectures, including ResNet50, Visual Geometry Group (VGG)16, VGG19, and InceptionV3, further highlights the superior sensitivity, specificity, and F1 score of the proposed framework. These findings underscore the transformative potential of diffusion models in enhancing dataset diversity, improving classification performance, and addressing data scarcity issues in medical imaging. The proposed framework offers a scalable, robust solution for brain tumor diagnosis, paving the way for improved disease prediction and treatment planning in clinical practice.

Primary familial brain calcification (PFBC) is a neurodegenerative disorder characterized by bilateral basal ganglia and dentate nuclei calcifications, with signs and symptoms often manifesting between 30 and 60 years, although many affected individuals remain asymptomatic. Herein, we present a 51-year-old male with bilateral basal ganglia and dentate nuclei calcifications found incidentally by brain computed tomography (CT) performed for sinus complaints. He had no associated signs or symptoms. The proband’s deceased mother’s last brain CT showed comparable brain calcifications. The proband’s daughter was being evaluated for neurologic signs and symptoms associated with abnormal lesions on brain magnetic resonance imaging. Her brain CT revealed bilateral basal ganglia calcifications. Genetic testing on the proband and his daughter revealed a novel heterozygous autosomal dominant mutation in the platelet-derived growth factor subunit B gene. Since most affected individuals are often past childbearing years before PFBC diagnosis, it is crucial to perform family planning and genetic counseling in consideration of family history.

Cerebral amyloid angiopathy (CAA) is a cerebral small vessel disease caused by the deposition of beta-amyloid in the small- and medium-sized blood vessels of the cerebral cortex and leptomeninges, leading to intracranial vascular amyloidosis. Herein, we report a case of CAA -related inflammation (CAA-ri), a rare clinical condition, focusing on the clinical manifestations, imaging characteristics, cerebrospinal fluid (CSF) findings, and treatment strategies. Key clinical manifestations included psychiatric abnormalities, cognitive impairment, and epilepsy. Brain magnetic resonance imaging revealed asymmetric white matter lesions, whereas susceptibility-weighted imaging demonstrated multiple microbleeds. CSF analysis indicated elevated total protein levels. Following corticosteroid pulse therapy, there was a marked improvement in both clinical symptoms and imaging findings. Given its rarity in clinical practice, early recognition and timely intervention of CAA-ri are crucial for optimizing patient outcomes and enhancing quality of life.