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Alzheimer's Disease (AD), a neurodegenerative disorder, is pathologically identified by amyloid plaques and neurofibrillary tangles composed of tau protein. AD pharmacotherapy aims to manage cognitive symptoms, delay disease progression, and treat behavioral symptoms. The treatment is primarily symptomatic and palliative, with no definitive disease-modifying therapy available. Cholinesterase inhibitors, including donepezil (Aricept), rivastigmine (Exelon), and galantamine (Razadyne), are...
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Amyloid fibrils are aggregates of misfolded proteins.  Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils. 
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Alzheimer's Disease (AD) is a continually advancing neurodegenerative disorder, distinguished by escalating memory loss, cognitive dysfunction, and dementia. The disease unfolds in three stages: preclinical, mild cognitive impairment (MCI), and dementia. Its onset is insidious, and the progression gradual, with the cause not well explained by other disorders.
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在抗粉胺治疗中缺失的环节

Pravat K Mandal1,2, Joseph C Maroon1, Rimil Guha Roy3

  • 1Department of Neurological Surgery, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania 15213, United States.

ACS chemical neuroscience
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概括

阿尔茨海默氏病可能与氧化应激和谷氨耗尽有关. 一种新的方法结合了lecanemab与谷氨前体玛-谷氨基氨基氨酸,以潜在地改善结果.

关键词:
阿尔茨海默氏症是阿尔茨海默氏症的一种疾病.抗粉类药物 抗粉类药物抗氧化剂 抗氧化剂是一种抗氧化剂.认知储备是一个认知储备.组合疗法是一种组合疗法.葡萄糖氨酸氨酸是什么?莱卡内马布 (lecanemab) 是一个氧化应激是一种氧化应激.

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科学领域:

  • 神经科学是一个神经科学.
  • 生物化学 生物化学
  • 老年学是指老年学的学科.

背景情况:

  • 阿尔茨海默病 (AD) 导致全球数百万人的认知能力显著下降.
  • 目前的AD研究和试验主要集中在β-粉样蛋白和tau假设上.
  • 莱卡尼马布显示了适度的认知延迟,但有显著的不良事件,如大脑胀和出血.

研究的目的:

  • 探索AD病变发生过程中的氧化应激 (OS) 假设.
  • 调查谷氨 (GSH) 枯竭在AD和轻度认知障碍 (MCI) 中的作用.
  • 提出一种新的阿尔茨海默病综合疗法.

主要方法:

  • 使用磁共振光谱 (MRS) 非侵入性测量大脑GSH水平.
  • 相关的海马GSH水平与记忆障碍.
  • 提出了一种治疗策略,将lecanemab与口服的玛-谷氨基半氨酸 (GGC) 结合起来.

主要成果:

  • 在MCI和AD患者的海马体中确认显著的GSH耗尽.
  • 观察到海马体GSH枯竭和记忆缺陷之间的正相关性.
  • 确定了lecanemab对有毒原纤维素和β-粉样蛋白清除的特异性.

结论:

  • 氧化应激和GSH耗尽可能是AD进展的早期事件.
  • 结合lecanemab和通过GGC补充GSH,可能会提供更有效的治疗策略.
  • 这种方法旨在减轻不良事件,并提高AD治疗的临床结果.