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This study investigates whether incorporating olfactory dysfunction into motor subtypes of Parkinson's disease (PD) improves associations with clinical outcomes. PD is commonly divided into motor subtypes, such as postural instability and gait disturbance (PIGD) and tremor-dominant PD (TDPD), but non-motor symptoms like olfactory dysfunction remain underexplored. We assessed 157 participants with PD using the University of Pennsylvania Smell Identification Test (UPSIT), Movement Disorder Society-Sponsored Revision of the Unified Parkinson's Disease Rating Scale (M-UPDRS), Montreal Cognitive Assessment (MoCA), 39-item Parkinson's Disease Questionnaire Summary Index (PDQ-39 SI), and 99mTc-TRODAT-1 imaging. Motor subtypes were categorized as PIGD and TDPD, and olfactory subtypes were categorized as total anosmia (TA) and non-anosmia (NA). Significant differences were observed, with the highest disease burden occurring in PIGD TA, while the lowest occurred in TDPD NA. The total M-UPDRS scores (59.0, 47.5, 43.0, 36.0; p < 0.001) and PDQ-39 SI scores (22.4, 22.8, 9.6, and 9.0; p < 0.001) varied significantly across groups, and the highest occurred for PIGD TA, followed by PIGD NA, TDPD TA, and TDPD NA. MoCA scores indicated the best cognitive performance in TDPD NA (p = 0.002). Thus, the results show that integrating olfactory dysfunction with motor subtypes may enhance PD classification, particularly in cognitive assessment in cases of TDPD. [ABSTRACT FROM AUTHOR]

Aims: Previous studies showed conflicting relationship between hyperlipidemia, lipid-lowering therapy and diabetic peripheral neuropathy (DPN). As most of these works emerges from the Western and Australian countries, our study aims to investigate whether hyperlipidemia or lipid-lowering therapy (LLT) is associated with DPN in Taiwanese patients with type 2 diabetes (T2D). Methods: A cross-sectional, hospital-based observation study in adults with T2D was conducted from January to October 2013. DPN was screened using the Michigan Neuropathy Screening Instrument. Data were obtained at the time of enrollment, including medication usage, anthropometric measurements and laboratory examinations. Results: 2,448 participants were enrolled, 524 (21.4%) of whom had DPN. Patients with DPN had significantly lower plasma total cholesterol (185.6 ± 38.6 vs 193.4 ± 42.3 mg/dL) and low-density lipoprotein cholesterol levels (114.6 ± 32.7 vs 119 ± 30.8 mg/dL). Multivariate analysis demonstrated that neither hyperlipidemia (adjusted OR (aOR), 0.81; 95% confidence interval (CI), 0.49–1.34) nor LLT (aOR, 1.10; 95% CI, 0.58–2.09) was associated with DPN. Subgroup analysis revealed that neither total cholesterol (aOR, 0.72; 95% CI, 0.2–2.62), low-density lipoprotein cholesterol levels (aOR, 0.75; 95% CI, 0.2–2.79), statin (aOR, 1.09; 95% CI, 0.59–2.03) nor fibrate (aOR, 1.73; 95% CI, 0.33–1.61) was associated with DPN. Conclusion: Our results suggest that neither hyperlipidemia nor lipid-lowering medication was associated with DPN in adults with T2D. DPN is a multifactorial disease, and our findings indicate that lipid metabolism may play a minor role in its pathogenesis. [ABSTRACT FROM AUTHOR]

Abstract Background Kainic acid (KA)-induced status epilepticus (SE) was involved with release of free radicals. Sesamin is a well-known antioxidant from sesame seeds and it scavenges free radicals in several brain injury models. However the neuroprotective mechanism of sesamin to KA-induced seizure has not been studied. Methods Rodents (male FVB mice and Sprague-Dawley rats) were fed with sesamin extract (90% of sesamin and 10% sesamolin), 15 mg/kg or 30 mg/kg, for 3 days before KA subcutaneous injection. The effect of sesamin on KA-induced cell injury was also investigated on several cellular pathways including neuronal plasticity (RhoA), neurodegeneration (Caspase-3), and inflammation (COX-2) in PC12 cells and microglial BV-2 cells. Results Treatment with sesamin extract (30 mg/kg) significantly increased plasma α-tocopherol level 50% and 55.8% from rats without and with KA treatment, respectively. It also decreased malondialdehyde (MDA) from 145% to 117% (p = 0.017) and preserved superoxide dismutase from 55% of the vehicle control mice to 81% of sesamin-treated mice, respectively to the normal levels (p = 0.013). The treatment significantly decreased the mortality from 22% to 0% in rats. Sesamin was effective to protect PC12 cells and BV-2 cells from KA-injury in a dose-dependent manner. It decreased the release of Ca2+, reactive oxygen species, and MDA from PC12 cells. Western blot analysis revealed that sesamin significantly reduced ERK1/2, p38 mitogen-activated protein kinases, Caspase-3, and COX-2 expression in both cells and RhoA expression in BV-2 cells. Furthermore, Sesamin was able to reduce PGE2 production from both cells under KA-stimulation. Conclusions Taken together, it suggests that sesamin could protect KA-induced brain injury through anti-inflammatory and partially antioxidative mechanisms.

Abstract Attenuation of inflammatory cell deposits and associated cytokines prevented the apoptosis of transplanted stem cells in a sciatic nerve crush injury model. Suppression of inflammatory cytokines by fermented soybean extracts (Natto) was also beneficial to nerve regeneration. In this study, the effect of Natto on transplanted human amniotic fluid mesenchymal stem cells (AFS) was evaluated. Peripheral nerve injury was induced in SD rats by crushing a sciatic nerve using a vessel clamp. Animals were categorized into four groups: Group I: no treatment; Group II: fed with Natto (16 mg/day for 7 consecutive days); Group III: AFS embedded in fibrin glue; Group IV: Combination of group II and III therapy. Transplanted AFS and Schwann cell apoptosis, inflammatory cell deposits and associated cytokines, motor function, and nerve regeneration were evaluated 7 or 28 days after injury. The deterioration of neurological function was attenuated by AFS, Natto, or the combined therapy. The combined therapy caused the most significantly beneficial effects. Administration of Natto suppressed the inflammatory responses and correlated with decreased AFS and Schwann cell apoptosis. The decreased AFS apoptosis was in line with neurological improvement such as expression of early regeneration marker of neurofilament and late markers of S-100 and decreased vacuole formation. Administration of either AFS, or Natto, or combined therapy augmented the nerve regeneration. In conclusion, administration of Natto may rescue the AFS and Schwann cells from apoptosis by suppressing the macrophage deposits, associated inflammatory cytokines, and fibrin deposits.