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Two primary symptom-relief drugs currently used to treat ALS patients are riluzole and edaravone. Riluzule acts as an NMDAR antagonist and edaravone functions as a scavenger of reactive oxygen species[68]. However, there remains an urgent need to develop effective disease-modifying therapies. Repurposing clinically available, FDA-approved drugs with known safety profiles and minimal organ toxicity, such as dantrolene, offers a promising strategy to accelerate clinical translation. This new formulation of dantrolene, Ryanodex, consists of crystalline nanoparticles[70]. While Ryanodex is FDA-approved for the treatment of malignant hyperthermia, its current application is intravenous, not intranasal[70]. A prior study failed to demonstrate efficacy of dantrolene in the same SOD1-G93A model[60], most likely due to its limited ability to cross the blood-brain barrier (BBB)[71]. Intranasal delivery of drugs, particularly in nanoparticle forms, has been well established to enhance BBB penetration, increasing drug concentration in the CNS and its retention time, thereby improving therapeutic efficacy while minimizing peripheral side effects and organ toxicity. This strategy is especially advantageous for treatment of long-term conditions, such as those involving chronic neurological diseases[72]. In fact, intranasal administration of riluzole nanoemulsions has been shown to produce higher brain concentrations than standard oral administration, enhancing its therapeutic potential in ALS[73]. Consistently, our previous studies demonstrated that intranasal administration of dantrolene nanoparticles in the Ryanodex formulation significantly increased brain concentration, prolonged drug duration, and enhanced the brain-to-blood concentration ratio compared to oral or subcutaneous administrations[62-64]. Intranasal dantrolene nanoparticles administered at the same dose (5mg/kg), daily, 5 days per week for up to 12 months, significantly inhibited memory loss in the 5XFAD Alzheimer’s disease mouse model, Discussion This study has demonstrated that intranasal dantrolene nanoparticles provide robust and significant therapeutic effects against motor neuron dysfunction, motor without evidence of side effects or nasal/liver toxicity[63, 74]. Given the chronic nature of ALS, the low systemic toxicity and high CNS penetration of intranasal dantrolene nanoparticle treatment further favor its utility for long-term treatment. In comparison with prior studies, the robust and significant neuroprotective and muscle-preserving effects observed in SOD1-G93A mice suggest enhanced drug delivery to the brain and spinal cord, with promoted efficacy in the CNS. Moreover, because ALS patients frequently develop difficult swallowing, intranasal drug delivery may be a more convenient and patient-friendly route of administration. A significant proportion of ALS patients develop cognitive impairment and depression-related psychiatric symptoms[75]. Accordingly, as intranasal dantrolene nanoparticles have demonstrated efficacy in treating memory dysfunction[63] and depressionand anxiety-like behaviors[76], this approach may offer additional clinical benefit beyond motor function preservation in the treatment of ALS. Similar to our previous findings in 5XFAD mice[63], the intranasal administration of vehicle alone (only the Ryanodex formulation) demonstrated predominantly minor, non-significant trends towards improvement in motor function, balance, and muscle strength, but to a clearly less effective degree than dantrolene-loaded nanoparticles. This suggests that dantrolene is the primary active agent providing neuroprotection and preserving muscle, although the potential additive role of the vehicle alone warrants further investigation. Although dantrolene is typically considered a muscle relaxant, it was not observed to impair 5XFAD mice[63]. In this ALS model, it significantly reversed muscle weakness, likely due to its motor neuron protection, causing reduced muscle denervation and potential direct protection against muscle damage. Overall, this preclinical study strongly supports the need for urgent clinical trials to evaluate the therapeutic potential of intranasal dantrolene nanoparticles in ALS patients.
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这项研究探讨了通过使用含有瑞安诺德(Ryanodex)配方载体(RFV)的鼻用氯化锂(LiCl)对5XFAD小鼠大脑中的炎症和焦亡(pyroptosis)进行抑制,并评估其对认知功能障碍和抑郁行为的治疗作用及副作用。

背景

本研究旨在评估鼻用氯化锂(LiCl)在瑞安诺德配方载体(RFV)中的治疗效果与副作用,重点关注其对5XFAD小鼠大脑中的炎症和焦亡的抑制作用,以及对认知功能和抑郁行为的改善作用。

方法

5XFAD小鼠和野生型(WT)B6SJLF1/J小鼠在2个月或9个月大时开始接受鼻用或口服氯化锂(3 mM/kg),氯化锂溶解在瑞安诺德配方载体(RFV)中,持续治疗12周。在5个月和12个月时,分别进行抑郁、认知、嗅觉和运动功能行为测试。每月监测体重。在6个月或13个月时,采集血液和大脑样本。通过ELISA测量甲状腺(TSH:甲状腺刺激激素)和肾脏(肌酐)功能的血液生物标志物。免疫印迹法检测老年小鼠大脑中类型1的Inositol 1,4,5-triphosphate受体(InsP3R-1)、氧化应激(4-HNE,MDA)、焦亡激活途径调节蛋白(NLRP3、切割型caspase-1、N-末端GSDMD)、促炎和神经保护细胞因子以及突触蛋白的蛋白质表达水平。

结果

与野生型小鼠相比,成年和老年5XFAD小鼠表现出明显的记忆丧失和抑郁行为,且这些行为通过鼻用LiCl在RFV中的治疗得到消除。鼻用LiCl在RFV中显著抑制了老年5XFAD小鼠大脑中InsP3R-1、氧化脂质修饰蛋白(MDA)以及由焦亡途径激活的蛋白(NLRP3、切割型caspase-1、N-末端GSDMD)的病理性增加,与老年野生型小鼠大脑相比。此外,鼻用LiCl在RFV中显著降低了细胞毒性细胞因子(IL-1β、IL-18、IL-6、TNF-α)的蛋白水平,缓解了星形胶质细胞和小胶质细胞的激活,增加了细胞保护性细胞因子IL-10的水平,并抑制了PSD-95突触蛋白的丧失。鼻用LiCl不影响血液中的TSH水平,但显著抑制了5XFAD小鼠血液中肌酐的异常年龄依赖性升高。鼻用LiCl在RFV中对体重、嗅觉和运动功能在WT或5XFAD小鼠中没有显著影响。

结论

鼻用LiCl在RFV中能够改善5XFAD小鼠的记忆丧失和抑郁行为,并且在长期使用中没有副作用或器官毒性。鼻用LiCl在RFV中有效抑制了老年5XFAD小鼠大脑中的氧化应激、炎症和焦亡。

https://pmc.ncbi.nlm.nih.gov/articles/PMC11712750/
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鼻内氯化锂(LiCl)一种很有前景的、非侵入性的脑部锂输送方法动物研究(如5xFAD小鼠模型)表明,该药物能有效治疗阿尔茨海默病(AD)和抑郁症的症状,其机制是通过减少炎症、氧化应激和细胞死亡(细胞焦亡/铁死亡),且全身副作用比口服锂更少。通过特定载体(如RFV)递送,该药物可靶向中枢神经系统,从而为利用锂的神经保护作用治疗神经系统和精神疾病提供一种更安全的方法。
工作原理
绕过全身毒性:鼻内给药可使氯化锂直接到达大脑,避免口服锂引起的全身高浓度副作用(肾脏、甲状腺问题)。
减少神经炎症:它能抑制大脑中的病理性炎症和细胞焦亡(炎症性细胞死亡),这是阿尔茨海默病进展的关键因素。
对抗氧化应激:氯化锂通过调节钙和铁的失调,防止氧化应激、线粒体功能障碍和铁死亡(铁依赖性细胞死亡)。
改善认知能力:在小鼠模型中,它能改善与阿尔茨海默病相关的记忆丧失和抑郁行为。
研究的主要发现
在 AD 模型中有效:鼻内 LiCl 在 Ryanodex 制剂载体 (RFV) 中显著改善了 5xFAD 小鼠(AD 模型)的记忆力并减轻了抑郁症状。
低毒性:与口服锂不同,这些模型中的长期使用未显示出明显的器官毒性。
直接脑部给药:研究测量发现,与口服给药相比,鼻内给药可使脑部与血清中的锂浓度比更高,证实了药物可直接进入中枢神经系统。
潜在应用
阿尔茨海默病:一种治疗认知能力下降及相关情绪问题的潜在方法。
抑郁症:可以缓解神经退行性疾病模型中出现的抑郁行为。
神经保护:提供了一种更安全地将锂已知的神经可塑性和保护作用传递到大脑的方法。
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鼻内丹特罗烯纳米颗粒对PS19 Tau转基因小鼠脑浓度和行为的影响  
在淀粉样转基因小鼠模型中,丹曲林被重新利用用于治疗阿尔茨海默病已被证明有效,但在陶氏症模型中尚未被研究。

目的:
研究了一种纳米颗粒鼻腔配方——鹰研究配方(Ryanodex,ERFR)在年轻成人和老年野生型及PS19 tau转基因小鼠中的效果。

方法:
鼻腔ERFR的生物利用度在2岁和9至11个月龄的C57BL/6J小鼠中进行了测量。在单次ERFR剂量后20分钟采集血液和脑部样本,并分析血浆和脑部浓度。在6个月和9个月龄的未治疗PS19 tau转基因小鼠中评估基线行为。PS19小鼠接受鼻腔ERFR治疗,可加或不加丙烯类(以增强认知功能障碍),治疗为期3个月,始于2个月大。研究了动物行为,包括认知(提示和情境恐惧条件训练、Y迷宫)、运动功能(旋转木)和嗅觉(埋藏食物测试)。

结果:
丹托林在血液和大脑中的浓度随着年龄增长下降,血液中浓度下降得更高,导致脑血浓度比更高。行为检测显示,即使使用丙烯醛,使用膉纶,在接受鼻腔ERFR慢性治疗后,PS19小鼠的认知、嗅觉或运动功能均无显著变化。

结论:
我们的研究表明,鼻腔给药ERFR在老年小鼠脑中的浓度高于血液,且在PS19小鼠中长期使用无严重的全身性副作用。  https://pmc.ncbi.nlm.nih.gov/articles/PMC11178503/
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鼻腔内给药丹曲林可增加脑部集中和持续时间    丹特罗烯已被证明对多种神经退行性疾病具有神经保护作用。然而,丹曲林在中枢神经系统的渗透有限,限制了其作为神经保护剂的效果。我们研究了丹曲林鼻腔内给药是否比常用口服方法更能更好地穿透大脑。C57BL/6小鼠,年龄2至4个月,接受了单剂量鼻腔或口服丹曲林(5mg/kg)。通过与P-gp/BCRP抑制剂、尼莫地平或依拉啶达联合给药,研究了丹曲林大脑清除的抑制效果。丹曲林在脑部和血浆中的浓度分别在给药后10、20、30、50、70、120、150和180分钟测量。不同组小鼠每周3次,分别给鼻腔服用丹曲林(5mg/kg)或载体,分别为3周或4个月,分别评估对嗅觉和运动协调的潜在不良反应。

我们发现鼻内给药180分钟后,脑内镒酮浓度持续维持,口服120分钟后浓度降至零。长期使用鼻腔用丹曲林未影响这些小鼠的嗅觉或运动功能。血脑屏障泵抑制剂并未进一步提高脑中丹托林峰值浓度。我们的结果表明,与口服相比,鼻内给药丹曲林是提高其大脑浓度和持续时间的有效途径,且对嗅觉或运动功能无明显副作用。https://pmc.ncbi.nlm.nih.gov/articles/PMC7065741/
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