Disulfidptosis in neurodegenerative diseases: From redox imbalance to neuronal dysfunction.

40 Hz light flicker stimulation for neurodegenerative diseases: Mechanisms and clinical perspectives.

ABSTRACT Background Chronic fatigue (CF) is increasingly prevalent, yet its role as an independent risk factor for cerebrovascular and neurodegenerative diseases remains underexplored. Objective This study aimed to prospectively assess the association between CF and the risks of Parkinson's disease (PD), Alzheimer's disease (AD), cerebral infarction (CI), and all-cause mortality (ACM). Methods We utilized data from 167,098 UK Biobank participants (aged 40–69) with baseline information on CF (≥6 months). Cox proportional hazards models with three tiers of covariate adjustment (demographics, lifestyle, comorbidities) were used to examine associations with incident PD, AD, CI, and ACM. Fine-Gray competing risk models accounting for death were also employed for PD, AD, and CI. Results CF was independently associated with significantly increased risks of PD (fully-adjusted HR = 3.02, 95% CI = 2.42–3.76, p < 0.0001), AD (HR = 1.68, 1.21–2.34, p = 0.002), CI (HR = 1.19, 1.02–1.39, p = 0.027), and ACM (HR = 1.86, 1.73–2.00, p < 0.0001). Competing risk analyses confirmed robustness (e.g. for PD: sHR = 2.97, p < 0.0001). Conclusions Chronic fatigue is an independent risk factor for developing PD, AD, CI, and for ACM. Assessment of CF may help identify high-risk populations for targeted prevention.

Functional cortical network alterations in Parkinson's disease with wearing-off revealed by resting-state fNIRS and graph theory.

The role of ultrasound in addressing neurodegenerative diseases: A review of mechanisms, applications, and challenges.

The oral-gut-brain axis is a path connecting the gastrointestinal tract and the central nervous system (CNS). The gut microbiota influences the immune system, metabolism, and nerve cells through the production of neurotransmitters and microbial metabolites that can cross the blood-brain barrier (BBB). The interplay between neuroinflammation and altered oral and gut microbiota is a bidirectional complex path modulated by inflammatory mediators. Recent studies suggest a potential role for Toll-like receptor (TLR) signaling pathways in the induction of neuroinflammation via the oral-gut-brain axis. As neuroinflammation is one of the key elements in the pathophysiology of neurodegenerative and neuropsychiatric disorders, this review was conducted to reflect on the pathophysiological pathways and clinical evidence on the role of TLR and inflammasome signaling pathways via oral-gut-brain axis in neurodegenerative diseases such as cognitive impairment, Alzheimer's disease, Multiple sclerosis, Parkinson's disease, Huntington's disease, and Amyotrophic lateral sclerosis, and psychiatric disorders such as major depressive disorder, anxiety disorders, schizophrenia, bipolar disorders, and Autism spectrum disorders. Because the contributing factors have not been fully understood yet, further studies could help provide novel therapeutic opportunities.

Differential cholinergic white matter microstructural alterations in multiple system atrophy and Parkinson's disease.

Cognitive impairment is a common manifestation of Parkinson's disease (PD) that can limit participation. A clearer understanding of how people with PD (PwPD) use strategies to support their functional cognition can guide interventions designed to promote occupational performance. To investigate strategy use by PwPD during a functional cognitive task and how it relates to task performance. Cross-sectional within and between groups. Participants' homes. PwPD without dementia (N = 51) were allocated into two groups according to Montreal Cognitive Assessment score: ≥26 for those with PD and normal cognition (PD-NC; n = 27) and ≤25 for those with PD and mild cognitive impairment (PD-MCI; n = 24). Performance outcomes (accuracy, total time, and efficiency) and strategy use on the Level 2 Adult/Older Adult version of the Weekly Calendar Planning Activity (WCPA). In the whole PD group, increased strategy use correlated with higher accuracy and longer total time, and four specific strategies correlated with higher accuracy (p < .04). The PD-NC group had higher accuracy and used more strategies than the PD-MCI group (p < .02), including three strategies associated with higher accuracy (cross off entered appointments, enter fixed appointments first, cross off free day; p < .03). In the PD-NC group, increased strategy use correlated with higher accuracy and longer total time (p < .02). Strategy use and WCPA performance outcomes did not correlate in the PD-MCI group (p > .10). This study adds to the understanding of how PwPD select and use strategies to support their functional cognition and suggests that PwPD could potentially benefit from interventions to optimize strategy use in occupational performance. Plain-Language Summary: People with Parkinson's disease experience changes in thinking and memory that affect their ability to participate in daily activities, and they use fewer strategies to support their cognition than their peers without Parkinson's disease. We investigated the strategies people with Parkinson's disease use to support their thinking and memory during a simulated functional activity, the Weekly Calendar Planning Activity. We sought to understand whether the strategies they used were related to better performance on the activity, and we explored differences in strategy use between people with Parkinson's disease with normal cognition and those with Parkinson's disease with possible mild cognitive impairment. We found that people with Parkinson's disease who used more strategies performed more accurately. Participants with Parkinson's disease with normal cognition used strategies that supported their accuracy but took longer to complete the task. Participants with Parkinson's disease with possible mild cognitive impairment used fewer strategies and ones that did not support their performance. Our findings indicate that people with Parkinson's disease may benefit from interventions focused on selecting and using strategies to improve their daily functioning.

To investigate the association between use of GLP-1 receptor agonists and incident Parkinson's disease. Cohort study using data from nationwide registers in Denmark, Norway and Sweden and an active-comparator, new-user design. We included 158 961 new users of GLP-1 receptor agonists and 188 065 new users of sulfonylureas, aged 45 years or older. Liraglutide accounted for 72.9% of GLP-1 receptor agonist follow-up time, followed by semaglutide (13.4%), exenatide (7.3%), dulaglutide (5.1%) and lixisenatide (1.3%). The primary outcome was incident Parkinson's disease, defined as a first-ever diagnosis of Parkinson's disease (ICD-10 G20) or Parkinson's disease dementia (ICD-10 F02.3) in national patient registers. Cox regression with propensity score weighting was used to estimate hazard ratios (HRs) and control for confounding. Mean age was 65 years and 43% were female. Incidence rates for Parkinson's disease were 5.2 and 8.0 per 10 000 person-years among GLP-1 receptor agonist and sulfonylurea users, respectively (adjusted HR 0.81 [95% CI 0.68-0.96]). Results were consistent in a 2-year lag-time analysis (HR 0.84 [95% CI 0.70-1.02]) after excluding or censoring users of DPP-4 inhibitors at cohort entry or during follow-up (HR 0.74 [95% CI 0.60-0.93]) and in subgroup analyses by sex and age. In this large observational cohort study, use of GLP-1 receptor agonists compared with sulfonylureas was associated with a lower risk of incident Parkinson's disease. These findings support a potential neuroprotective role of GLP-1 receptor agonists, though replication in additional studies is needed.

The impact of ageing and rurality on the use of medical services in Parkinson's disease: A data linkage study using the 45 and Up Study and Medicare Benefits Schedule.

Lnc-USP28-6/ZBTB16 axis orchestrates NLRP3 inflammasome activation and α-synuclein SUMOylation to drive Parkinson's disease pathogenesis.

Interplay of age-sensitive cortical vulnerability and dopaminergic degeneration in clinical manifestations of Parkinson's disease.

Cognitive processes and neurophysiological mechanisms of time processing in Parkinson's disease: A narrative review.

State-dependent gut-brain electrophysiological coupling tracks motor complication severity in Parkinson's disease.

Combination of CSF α-synuclein seed amplification assay and amyloid-β42 predicts cognitive decline in Parkinson's disease.

Elucidating the molecular mechanisms underlying the therapeutic effects of 6-shogaol on Parkinson's disease.

Balenine alleviates neurodegeneration and inflammation in a mouse model of Parkinson's disease.

Safety and efficacy of staged, bilateral magnetic resonance-guided focused ultrasound pallidothalamic tractotomy for motor complications of Parkinson's disease: a prospective, multicentre, single-arm trial.

Machine learning based multi-omics analysis reveals key molecular determinants of Parkinson's disease severity.

Branched-chain amino acids alleviate Parkinson's neurodegeneration via microbial propionate-dependent restoration of the PI3K/Akt/mTORC1 axis.