AIMS Neuroscience最新文献

Dementia cases are projected to triple globally by 2050, largely driven by an aging population. While aging remains the primary risk factor, emerging evidence suggests that diet, including total meat supply, may influence dementia risk. This study investigates the relationship between total meat supply (red and white meat) and dementia incidence using data from 204 countries. Bivariate correlations revealed a significant positive association between total meat supply and dementia incidence globally (r = 0.59, p < 0.001), with a stronger effect observed in low- and middle-income countries (z = 3.92, p < 0.001). Partial correlation analyses and multiple regression models, controlling for aging, economic status, genetic predisposition, and urbanization, confirmed that meat supply remained a significant predictor of dementia (Beta = 0.20, p < 0.001). Aging showed the strongest influence (Beta = 0.79, p < 0.001), underscoring its dominant role. Regional analyses suggested socio-economic disparities, dietary habits, and limited access to diverse nutrition as factors amplifying the association in developing regions. These findings identify total meat supply as a modifiable dietary factor contributing to dementia risk, particularly in resource-constrained settings. Implementing tailored dietary interventions may help reduce dementia incidence globally, especially in vulnerable populations.

Infantile neuroaxonal dystrophy (INAD), also known as PLA2G6-associated neurodegeneration (PLAN), is a rare, early-onset, autosomal recessively inherited neurodegenerative disease belonging to the group of neurodegenerations with brain iron accumulation (NBIA). The main cause of this disease is bi-allelic mutations in the PLA2G6 gene, which codes for the enzyme phospholipase A2 type VI. Clinically, it manifests with progressive neurodevelopmental impairment, psychomotor regression, movement disorders, and pyramidal signs. Initially described in the 1950s, the classical form presents in the first two years of life, although later-onset variants are recognized. At the neuropathological level, INAD is characterized by the presence of neuroaxonal spheroids, which are dilations of degenerated axons, located mainly in the white matter, basal ganglia, and cerebellum. INAD is considered a rare or ultra-rare disease, with an estimated prevalence of approximately 1 per million individuals. Diagnosis requires a comprehensive evaluation combining clinical with neuroimaging studies, mainly magnetic resonance imaging (MRI), and genetic analysis. MRI may reveal early cerebellar atrophy and a low-intensity signal in the globus pallidus on iron-sensitive sequences, indicative of iron accumulation. Currently, there is no curative treatment for INAD, so management focuses on providing palliative care and symptom control using a multidisciplinary approach. However, various therapeutic strategies are being investigated, including gene therapy to correct the genetic defect, as well as approaches to modulate pathological pathways such as lipid peroxidation and iron accumulation.

Young adulthood is a critical period marked by significant cognitive demands, requiring efficient brain function to manage academic, professional, and social challenges. Many young adults struggle with focus, stress management, and information processing. Emerging research suggests that auditory stimulation, specifically binaural beats and white noise, may enhance cognitive abilities and address these challenges. This exploratory study investigates the immediate effects of alpha binaural beats (ABB) and alpha binaural beats combined with white noise (AWN) on brain connectivity in young adults using functional magnetic resonance imaging (fMRI). Twenty-nine participants (n = 14 ABB, n = 15 AWN; mean age ≈ 22.14 years) were randomly assigned to receive either ABB or AWN during fMRI scans. Using dynamic independent component analysis (dyn-ICA), we examined the modulation of functional brain circuits during auditory stimulation. Preliminary findings revealed distinct and overlapping patterns of brain connectivity modulation of ABB and AWN. ABB primarily modulated connectivity within circuits involving frontoparietal, visual-motor, and multisensory regions, potentially enhancing cognitive flexibility, attentional control, and multisensory processing. Conversely, AWN primarily modulated connectivity in salience and default mode networks, with notable effects in limbic or reward regions, suggesting enhancements in focused attention and emotional processing. These preliminary results demonstrate that ABB and AWN differentially modulate brain networks on an immediate timescale. ABB may promote cognitive adaptability, while AWN enhances focused attention and emotional stability. Although behavioral effects were not assessed, these findings provide a neurobiological basis for understanding how these stimuli impact brain circuits. These preliminary findings may aid the development of personalized strategies for cognitive and emotional well-being. Given the exploratory nature, small sample size, and lack of concurrent behavioral data, these findings should be interpreted cautiously. Future research with rigorous designs, including control groups and behavioral measures, is needed to explore the long-term effects and applications of these interventions in various settings.

Neuromodulation techniques have emerged as valuable strategies for patients with depression and anxiety who do not respond to traditional therapies. Repetitive transcranial magnetic stimulation (rTMS) and transcranial direct current stimulation (tDCS) treatments are heterogeneous; however, they all share an average duration of at least 10 days, thus requiring significant patient commitment to maintain adequate compliance. Here we describe a 68-year-old woman who suffered from depression and generalized anxiety disorder and underwent a short-intensive combined protocol, thus highlighting its effectiveness and good tolerability.

Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is an autoimmune inflammatory demyelinating disorder that can manifest as optic neuritis, transverse myelitis, and acute disseminated encephalomyelitis. Although typically monophasic, relapsing cases are more common in adults. Current treatments include corticosteroids, intravenous immunoglobulin, immune-suppressive drugs, and plasma exchange, but there is emerging interest in the use of interleukin-6 (IL-6) inhibitors to prevent relapses such as tocilizumab and satralizumab. This review analyzed 24 studies on IL-6 inhibitors for MOGAD, including case reports, case series, and retrospective studies with at least one MOGAD patient. Tocilizumab demonstrated significant efficacy, with most studies reporting reduced annualized relapse rates (ARR), prolonged relapse-free periods, and improved neurological outcomes, including stabilization or recovery of vision, motor function, and magnetic resonance imaging (MRI) lesion resolution. Satralizumab also showed potential, though data were more limited. While IL-6 inhibitors appear beneficial for steroid-dependent or treatment-resistant MOGAD, the existing data are limited to small, observational studies. Larger controlled trials are needed to establish their long-term efficacy and safety.

Scientific investigations have increasingly revealed the intricate connection between masticatory function and cognitive functioning, as well as psychological well-being. Addressing malocclusions, such as the common unilateral posterior crossbite, during early developmental stages, emerges as an effective strategy for gaining health. This study aims to evaluate the efficacy of treating unilateral posterior crossbite by utilizing a function generating bite (FGB) appliance in a 12-year-old child, focusing on its impact on specific cognitive domains. Through meticulous pre- and post-treatment assessments, encompassing global cognitive activity (Colored Progressive Matrices), verbal and spatial working memory (Digit Span and Corsi Block-Tapping Test), and graphic fluency (modified Five Points Test), this research aims to elucidate the cognitive benefits associated with FGB treatment. Results unveil that a mere seven-month application of FGB effectively rectified the malocclusion while concurrently yielding notable improvements in the cognitive abilities under scrutiny. Additionally, post-treatment observations revealed enhanced well-being and sleep quality, further emphasizing the multifaceted benefits of such interventions. Although this study presents findings from a singular case, it serves as a catalyst for further exploration into the intricate interplay between masticatory function and cognitive performance. Such endeavors are vital for advancing holistic healthcare practices that integrate dental care with cognitive and psychological considerations, thereby fostering comprehensive well-being and optimal development.

Epigenetics is the study of how cells control gene activity without changing the DNA sequence. Epigenetic changes affect how genes are turned on and off or expressed, and thus help regulate how cells in different parts of the body use the same genetic code. Errors in the epigenetic process can not only lead to abnormal gene activity or inactivity, but can also influence alternative splicing (AS) and could cause human diseases. Understanding of how epigenetic defects can affect human health, especially for neurological disorders, could suggest targets for therapeutic interventions. For such a purpose, the Lesch-Nyhan disease (LND) has been selected as a valuable model to study the genetic-epigenetic interplay, especially to explore the epistasis between the housekeeping hypoxanthine phosphoribosyltransferase 1 (HPRT1) and β-amyloid precursor protein (APP) genes. This review is structured as follows: we begin with an overview about the monogenetic neurological disorders associated with epigenetic changes; next, the current knowledge on HPRT1 and APP genes is provided; then, the epistasis between HPRT1 and APP genes related to the neurobehavioral syndrome in LND is described; and finally, we present the construction of expression vectors to study intermolecular interactions between the hypoxanthine-guanine phosphoribosyltransferase (HGprt) enzyme and APP in LND. Information obtained from such expression vectors would be useful for future directions to design therapies through epigenetic interventions.

Alzheimer's Disease (AD) remains a significant global health challenge, characterized by progressive neurodegeneration and a decline in cognitive abilities such as memory and learning. Despite being the main cause of dementia worldwide, the precise mechanisms that underlie neuronal dysfunction and synaptic plasticity impairment in AD remain elusive. However, while genetic mutations, dietary factors, and immune dysregulation are implicated in AD pathogenesis, the current therapeutic approaches are largely centered around acetylcholinesterase inhibitors (AChEIs). Nevertheless, this cholinergic hypothesis of AD is no longer satisfactory in describing this disease and has demonstrated a limited efficacy. Hence, new treatment approaches should be developed, and that requires us to view AD from a new perspective. Herein, in our review, we present the latest studies that discussed possible AD pathologies and pharmacotherapies. Additionally, we highlight that the emerging treatments that precisely targets brain regions associated with enhancing neuroplasticity have delivered promising results and seem to be more effective than older treatments. Finally, by viewing AD as a complex interplay of various factors that ultimately cause synaptic dysfunction and cognitive decline, we can develop more effective therapeutic interventions and ultimately alleviate the significant burden of this debilitating disease for both patients and their families.

Parkinson's Disease is a neurodegenerative central nervous system (CNS) disease that primarily affects the dopaminergic cells of the Substantia Nigra in the midbrain and causes a diverse array of symptoms, including dystonia, a loss of balance, difficulty initiating movements, akinesia, muscle spasms, and tremors. It has long been known that environmental and commercial compounds are linked to an increased risk of Parkinson's Disease. Of importance, gluten, a complex polysaccharide, has been hypothesized to cause some of the symptoms related to Parkinson's Disease. It is hypothesized that gluten causes a chronic inflammatory state which may lead to plaque formation and neuronal cell death in the substantia nigra, alongside the symptoms of Parkinson's Disease. This literature review hopes to explore the relationship gluten has as an inflammatory molecule and its role in the production and prolongation of the disease processes in Parkinson's Disease.

Disorders of the metabolism, including obesity and type 2 diabetes, represent significant global health challenges due to their rising prevalence and associated complications. Despite existing therapeutic strategies, including lifestyle interventions, pharmacological treatments, and surgical options, limitations such as poor adherence, side effects, and accessibility issues call attention to the need for novel solutions. Tetrahydrocannabivarin (THCV), a non-psychoactive cannabinoid derived from Cannabis sativa, has emerged as a promising agent to manage metabolic disorders. Unlike tetrahydrocannabinol (THC), THCV exhibits an antagonistic function on the CB1 receptor and a partial agonist function on the CB2 receptor, thus enabling appetite suppression, enhanced glucose regulation, and increased energy expenditure. Preclinical studies demonstrated that THCV improves insulin sensitivity, promotes glucose uptake, and restores insulin signaling in metabolic tissues. Additionally, THCV reduces lipid accumulation and improves the mitochondrial activity in adipocytes and hepatocytes, shown through both cell-based and animal research. Animal models further revealed THCV's potential to suppress appetite, prevent hepatosteatosis, and improve metabolic homeostasis. Preliminary human trials support these findings, thereby showing that THCV may modulate appetite and glycemic control, though larger-scale studies are necessary to confirm its clinical efficacy and safety. THCV's unique pharmacological profile positions it as a possible therapeutic candidate to address the multifaceted challenges of obesity and diabetes. Continued research should concentrate on optimizing formulations, undertaking well-designed clinical studies, and addressing regulatory hurdles to unlock its full potential.