Age-related neurodegenerative disorders encompass a range of diseases in the central nervous system characterized by neuronal death, disrupted neural connections, altered neurotransmitter secretions, and notable features of proteinopathy. The increasing prevalence of age-related neurodegenerative diseases (NDs) highlights the need for effective therapeutic strategies. This review aims to advocate for non-pharmacological interventions (NPIs), such as adopting healthy lifestyle habits, engaging in physical exercises, ensuring sufficient quality sleep, and maintaining cognitive activity, over pharmacological treatments. A literature search was conducted across PubMed, Scopus, Web of Science, and Google Scholar. Studies were included if they focused on NPIs in ND treatment, were published in peer-reviewed journals, and were written in English. Compared to pharmacological options, many of the NPIs have demonstrated satisfactory clinical outcomes in delaying the progression of neurodegenerative disorders or preventing them in certain cases. Specific dietary patterns, such as the Mediterranean-Dietary Approaches to Stop Hypertension Diet Intervention for Neurodegenerative Delay and Mediterranean diet, have been shown to reduce cognitive impairment while mitigating neuroinflammation and oxidative stress. Regular physical exercise promotes an anti-inflammatory state and enhances the secretion of anti-stress hormones like dopamine, thereby fostering neuroplasticity. In addition, obtaining adequate quality sleep and adhering to a consistent circadian rhythm is crucial for memory consolidation and overall cognitive health. Moreover, stress management techniques, such as meditation and yoga, improve cerebral blood flow and help preserve brain structure. Cognitive training and social engagement further contribute to the delay and attenuation of neurodegeneration, thus maintaining cognitive health. Although NPIs show promise in slowing ND progression, further research is needed to validate their effectiveness.

Lisdexamfetamine (LDX) is a d-amphetamine prodrug with a long-acting therapeutic profile. It has become well-known in recent years due to its widespread use in treating several psychological disorders, such as attention-deficit/hyperactivity disorder and binge eating disorder. However, concerns have been raised about its potential neurotoxic properties, particularly with long-term use. Although direct evidence of LDX-induced neurotoxicity is limited, insights can be drawn from studies on the harmful impacts of its parent compound and related amphetamines, such as amphetamine and methamphetamine, on the central nervous system. The potential mechanisms through which these drugs exert their neurotoxic effects include mitochondrial dysfunction, oxidative stress, neuroinflammation, synaptic failure, and excitotoxicity, all of which contribute to neuronal injury and death. Furthermore, amphetamines have been shown to disrupt the blood-brain barrier, likely triggered by the aforementioned mechanisms, with neuroinflammation being the most significant factor. In this review, we aim to synthesize the available knowledge on the potential mechanisms behind LDX-induced neurotoxicity and emphasize the need for future studies to better understand the long-term side effects of LDX.

Post- stroke depression (PSD) is the most common psychological complication among stroke survivors and is strongly associated with poor outcomes and increased mortality. Acupuncture has been proposed as a potential treatment for PSD. In this overview, 13 meta-analyses (MAs) of randomized controlled trials published up to August 2023 that evaluated acupuncture for PSD were identified. Across these MAs, acupuncture generally demonstrated greater efficacy than control interventions in alleviating depressive symptoms. However, methodological assessment using the A MeaSurement Tool to Assess Systematic Reviews 2 (AMSTAR-2) rated all included studies as having critically low quality, indicating pervasive design and reporting weaknesses. Reporting quality, as evaluated by the Preferred Reporting Items for Systematic Reviews and MAs guidelines, was relatively high, with over 90% of checklist items being rated “yes” or “partially yes.” When the quality of evidence was appraised through the grading of recommendations assessment, development, and evaluation system, only nine of 61 outcomes were classified as moderate quality, 29 as low quality, and the remainder as very low quality. Although acupuncture appears to be a safe and potentially beneficial option for managing PSD, the overall strength of evidence remains limited. Thus, these findings should be interpreted with caution. Future research should prioritize rigorous trial design, standardized intervention protocols, and comprehensive meta-analytic methods to enhance the reliability and clinical applicability of evidence on acupuncture for PSD.

Ischemic stroke is the most prevalent and severe form of cerebrovascular disease and a leading cause of significant neurological disability. As the primary cause of hospitalization for neurological disorders, it necessitates urgent and effective therapeutic interventions. Xijiao Dihuang decoction (XJDHT), a classical traditional Chinese medicinal formula, is traditionally known for its effects in heat clearing, detoxification, blood cooling, and blood stasis removing. Emerging evidence suggests its potential to promote neurological recovery following ischemic stroke; however, systematic evaluation remains limited. This study employed a systematic network pharmacology approach to elucidate the molecular mechanisms underlying XJDHT’s therapeutic effects on ischemic stroke. LC-MS identified 24 bioactive compounds in XJDHT, using Traditional Chinese Medicine Systems Pharmacology and SwissTargetPrediction databases for target prediction. Disease targets for ischemic stroke were retrieved from GeneCards, Online Mendelian Inheritance in Man, Therapeutic Target Database, and Gene Expression Omnibus datasets. Intersection analysis found 424 overlapping targets between 690 compound targets and 3415 disease targets. Cytoscape and STRING platforms were used to construct networks and identify hub genes and critical modules. Functional enrichment analysis was conducted using the Database for Annotation, Visualization, and Integrated Discovery database. Network analysis identified core bioactive constituents, including paeoniflorin, albiflorin, benzoylpaeoniflorin, kaempferol, paeonol, ellagic acid, pinostrobin, β-sitosterol, and stigmasterol. Key therapeutic targets comprised phosphatidylinositol-4,5-bisphosphate 3-kinase regulatory subunit 1, SRC proto-oncogene, signal transducer and activator of transcription 3, phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha, phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit beta, phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta, AKT serine/threonine kinase 1, epidermal growth factor receptor, estrogen receptor 1, Harvey rat sarcoma virus, and neuroblastoma RAS viral oncogene homolog. The Kyoto Encyclopedia of Genes and Genomes pathway enrichment revealed significant involvement in the mammalian target of rapamycin signaling pathway, mitogen-activated protein kinase cascade, phosphatidylinositol 3-Kinase-Protein Kinase B (PI3K-AKT) pathway, erythroblastic leukemia viral oncogene homolog signaling, and vascular endothelial growth factor-mediated angiogenesis. These findings suggest XJDHT exerts neuroprotective effects through coordinated modulation of inflammatory responses and cellular signaling cascades, exhibiting the characteristic therapeutic properties of a multicomponent, multitarget, and multipathway approach.

Central visual conduction ability is crucial to human perception and visual skills. In sports, for instance, it enables athletes to gather information, predict movements, make quick decisions, and perform precise motor actions. In the present study, modern electrophysiological tools, such as visual evoked potentials (VEPs), were employed to assess central visual transmission. The goal was to analyze three VEP waveforms (N75, P100, and N145) in male athletes (n = 100) from cricket, yogasana, karate, and gymnastics, together with a control group of physically active boys without specific training in these disciplines. For the P100 waveform, yogasana and karateka practitioners showed significantly shorter latencies compared to all other groups (p<0.05), followed by cricketers, who had latencies similar to gymnasts. The N75 waveform for yogasana and karate practitioners showed significantly faster transmission times than the cricket and control groups (p˂0.05). Furthermore, the N75 waveform for the left eye in gymnasts had shorter latency compared to cricketers and controls. The N145 wave for the right eye in yogasana and karate practitioners had shorter latencies compared to those of other athletes (p<0.05). Meanwhile, karatekas showed higher amplitudes than those practicing yogasana and the controls, indicating that training experience might be a key factor. This study provides valuable insights into the unique visual processing demands and capabilities of athletes in various disciplines. Yogasana and karate, being gaze-oriented practices that integrate mind-body control, showed shorter latency across all groups, followed by ocularly dominant cricketers, visually trained gymnasts, and controls.

The rates of incidence and progression of Alzheimer’s disease (AD) vary significantly among post-menopausal women. However, the mechanisms that underlie this phenomenon remain obscure. Here, we established the high-fat diet-fed ovariectomized (OVXHF) mouse model and observed significant memory deficits in this model. Using 16S rDNA sequencing, we found that OVXHF mice displayed higher biodiversity and a distinct gut microbiome composition compared with normal chow-fed mice. Functional analysis further revealed that genes associated with the iron complex transport system and ATP-binding cassette are differentially expressed in OVXHF mice. Moreover, normal fecal microbiota transplantation (FMT) successfully restored the cognitive impairments in OVXHF mice through rebalancing the gut microbiota. In particular, the Bacteroides-to-Prevotella ratio was significantly increased in OVXHF mice but rescued by FMT. Altogether, these results suggest that an imbalance between Bacteroides and Prevotella in the gut microbiota accelerates the process of cognitive dysfunction in postmenopausal women on a high-fat diet.

Parkinson’s disease (PD) is a progressive neurodegenerative disorder, and the relationship between oxidative stress and PD is complex and multifaceted. Recent research has demonstrated that protocatechuic acid (PCA) and karanjin (KJN) can mitigate oxidative stress and may offer neuroprotective benefits in PD. PCA has also been reported to work synergistically with various other drugs or phytoconstituents, such as PCA and ginkgolide B in neuroprotection, PCA with catechin and vanillic acid against bacterial adhesion, and PCA with 5-fluorouracil in cancer therapy. 1-methyl-4-phenylpyridinium (MPP+) was used to induce PD in SH-SY5Y cells, leading to increased intracellular reactive oxygen species (ROS) generation and significant cell damage. Treatments with KJN and PCA reduced MPP⁺-induced cell damage by decreasing ROS generation. KJN and PCA enhanced NRF2 mRNA and heme oxygenase-1 (HO-1) expression. However, the HO-1 inhibitor zinc protoporphyrin diminished the antioxidant and neuroprotective benefits of KJN and PCA. NRF2 knockdown decreased HO-1 expression and the neuroprotective effects of KJN and PCA. The phosphoinositide 3-kinase/Akt inhibitor LY294002 eliminated the impact of KJN and PCA on NRF2-HO-1 expression, cell survival, lactate dehydrogenase release, and ROS production in MPP⁺- stimulated SH-SY5Y cells, but not the MAPK pathway inhibitors (PD98059, SP600125, and SB203580). These findings suggest that the neuroprotective effects of KJN and PCA in SH-SY5Y cells are linked to NRF2-mediated HO-1 expression, specifically through the PI3K/Akt pathway.

Research on cerebrovascular stroke and its predictors in chronic kidney disease (CKD) patients is limited compared to cardiovascular studies. In this study, we aimed to investigate the frequency, types, risk factors, and symptoms of ischemic brain infarctions in CKD patients. This observational study involved 155 adults with CKD, with an average age of 55.36 ± 4.28 years; 70 were males and 85 were females. The mean duration of uremia was 6.40 ± 1.36 years. Among the included patients, 71% were receiving hemodialysis. All participants underwent neurological assessment, laboratory testing, carotid duplex ultrasonography, and brain magnetic resonance imaging. The prevalence of silent ischemic brain infarctions was high at 78.7% (n = 122), with a higher occurrence among end-stage kidney disease patients (n = 110) compared to those not on dialysis (p=0.0001). About 19.7% (n = 24) developed focal stroke symptoms, while 63.2% (n = 98) were asymptomatic. Neurological symptoms included dysarthria, hemihypoesthesia, hemianopia, parkinsonism, and choreo-dystonia. Regression analysis revealed that brain infarctions were linked to severity of CKD (odds ratio [OR] = 6.32, 95% confidence interval [CI] = 3.20-15.45, p=0.0001), hypertension (OR = 8.34, 95% CI = 5.46-16.25, p=0.0001), hypertriglyceridemia (OR = 5.20, 95% CI = 2.45-12.33, p=0.001), hyperuricemia (OR = 3.40, 95% CI = 1.40-6.32, p=0.001), anemia (OR = 2.43, 95% CI = 1.60-5.28, p=0.01), hypoalbuminemia (OR = 3.25, 95% CI = 1.64-8.42, p=0.01), and albuminuria (OR = 2.53, 95% CI = 1.20-5.42, p=0.03). Persistent brain damage led to poor clinical outcomes in stroke patients. In conclusion, CKD patients face an elevated risk of ischemic brain infarctions and stroke, with various vascular and non-vascular risk factors playing a role. Management strategies should focus on correcting metabolic abnormalities, addressing underdiagnosed risk factors, and implementing preventive measures to reduce the risk of recurrent strokes.

Guillain- Barré syndrome (GBS) is an autoimmune inflammatory neuropathy frequently triggered by infections such as the Epstein-Barr virus and influenza B virus. While cranial nerve involvement occurs in nearly half of the cases, atypical presentations, including paraplegia with bilateral facial nerve palsy, are extremely rare. Herein, we report a 42-year-old female presenting with progressive lumbosacral pain, paraplegia, and bilateral facial nerve palsy. Diagnostic findings included demyelinating changes on electromyography, protein-cell separation in cerebrospinal fluid, and elevated anti-sulfatide immunoglobulin (Ig)G antibodies, confirming acute inflammatory demyelinating polyneuropathy. Treatment with intravenous Ig and adjunct therapies resulted in significant recovery and improved quality of life. This case emphasizes the diagnostic role of anti-sulfatide antibody testing in atypical GBS and highlights the potential of sulfatide-targeted therapies as novel interventions.

A 40-year-old female patient with refractory musicogenic epilepsy and non-lesional magnetic resonance imaging neuroimaging is highlighted in this report. A right temporal lobectomy was necessary and sufficient to effect a durable surgical cure without recurrence for over approximately 18 years in follow-up while remaining off seizure medications for the prior 16 years. Our case report delineates that this patient was cured with a surgical resection guided by metabolic neuroimaging. This patient was evaluated for cerebral localization of seizure onsets to guide further therapy in an epilepsy center and the evaluation for localization of seizure onset identified that Ictal single photon emission computed tomography (SPECT) imaging identified an approximately 25% increase in blood flow or metabolism in the right temporal lobe during seizures compared with the baseline. Seizure semiology and electroencephalography localization were concordant with SPECT localization.