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探索阿尔茨海默病的治疗前景:当前策略与未来方向

Navigating the treatment landscape of Alzheimer's disease: Current strategies and future directions.

作者信息

Mohapatra Tapas Kumar, Nayak Reena Rani, Ganeshpurkar Ankit, Tiwari Prashant, Kumar Dileep

机构信息

Department of Pharmacology Nityananda College of Pharmacy Seragarh Balasore Odisha India.

Department of Pharmaceutical Chemistry Nityananda College of Pharmacy Balasore Odisha India.

出版信息

Ibrain. 2025 May 10;11(2):162-184. doi: 10.1002/ibra.12197. eCollection 2025 Summer.


DOI:10.1002/ibra.12197
PMID:40546882
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12177682/
Abstract

Alzheimer's disease (AD), a neurodegenerative disease leading to dementia, lacks a single definitive diagnosis. While current medications only manage symptoms, the ideal treatment would restore cognition. Traditional therapies targeting beta-amyloid haven't yielded significant results, while new approaches target tau protein tangles, protein degradation pathways, inflammation, and neurotrophic factor depletion. Autophagy, a cellular degradation and recycling process, has emerged as a crucial hallmark and contributor to the pathogenesis of AD. Notably, autophagy induction has emerged as a promising therapeutic approach, with inducers like celastrol and caudatin promoting the degradation of toxic protein aggregates. Additionally, innovative drug formulations, such as nanoparticles, are being explored for targeted drug delivery. Research is increasingly focusing on neuroinflammation and developing multi-targeted drugs to address various aspects of AD, potentially leading to preventive strategies in the early stages. This review summarizes the current state and emerging trends in AD drug development.

摘要

阿尔茨海默病(AD)是一种导致痴呆的神经退行性疾病,目前尚无单一的确切诊断方法。虽然目前的药物只能控制症状,但理想的治疗方法是恢复认知功能。针对β-淀粉样蛋白的传统疗法并未取得显著成效,而新的治疗方法则针对tau蛋白缠结、蛋白质降解途径、炎症和神经营养因子耗竭。自噬是一种细胞降解和再循环过程,已成为AD发病机制的一个关键标志和促成因素。值得注意的是,自噬诱导已成为一种有前景的治疗方法,如雷公藤红素和尾叶香茶菜素等诱导剂可促进有毒蛋白质聚集体的降解。此外,正在探索创新的药物制剂,如纳米颗粒,用于靶向药物递送。研究越来越关注神经炎症,并开发多靶点药物来解决AD的各个方面问题,这可能会在早期阶段带来预防策略。本综述总结了AD药物研发的现状和新趋势。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72b8/12177682/14e4d5515ef9/IBRA-11-162-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72b8/12177682/20a248d63e0e/IBRA-11-162-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72b8/12177682/a32fc1e59424/IBRA-11-162-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72b8/12177682/5fb07706f064/IBRA-11-162-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72b8/12177682/14e4d5515ef9/IBRA-11-162-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72b8/12177682/20a248d63e0e/IBRA-11-162-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72b8/12177682/a32fc1e59424/IBRA-11-162-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72b8/12177682/5fb07706f064/IBRA-11-162-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72b8/12177682/14e4d5515ef9/IBRA-11-162-g001.jpg

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[1]
Navigating the treatment landscape of Alzheimer's disease: Current strategies and future directions.

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[4]
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[6]
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[7]
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[8]
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本文引用的文献

[1]
Molecular engineering of a theranostic molecule that detects Aβ plaques, inhibits Iowa and Dutch mutation Aβ self-aggregation and promotes lysosomal biogenesis for Alzheimer's disease.

J Mater Chem B. 2024-8-7

[2]
Aspartame Causes Developmental Defects and Teratogenicity in Zebra Fish Embryo: Role of Impaired SIRT1/FOXO3a Axis in Neuron Cells.

Biomedicines. 2024-4-12

[3]
Interaction of Tau with Kinesin-1: Effect of Kinesin-1 Heavy Chain Elimination on Autophagy-Mediated Mutant Tau Degradation.

Biomedicines. 2023-12-19

[4]
Corynoxine promotes TFEB/TFE3-mediated autophagy and alleviates Aβ pathology in Alzheimer's disease models.

Acta Pharmacol Sin. 2024-5

[5]
Fe65-engineered neuronal exosomes encapsulating corynoxine-B ameliorate cognition and pathology of Alzheimer's disease.

Signal Transduct Target Ther. 2023-10-23

[6]
PPARɑ Ligand Caudatin Improves Cognitive Functions and Mitigates Alzheimer's Disease Defects By Inducing Autophagy in Mice Models.

J Neuroimmune Pharmacol. 2023-9

[7]
Anti-Amyloid Immunotherapies for Alzheimer's Disease: A 2023 Clinical Update.

Neurotherapeutics. 2023-7

[8]
Prevalence and modifiable risk factors for dementia in persons with intellectual disabilities.

Alzheimers Res Ther. 2023-7-18

[9]
CGRP physiology, pharmacology, and therapeutic targets: migraine and beyond.

Physiol Rev. 2023-4-1

[10]
ApoE in Alzheimer's disease: pathophysiology and therapeutic strategies.

Mol Neurodegener. 2022-11-8

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