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Impairment of the autophagy-lysosomal pathway in Alzheimer’s diseases: Pathogenic mechanisms and therapeutic potential

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Acta Pharmaceutica Sinica B 2022年第3期12卷 1019-1040页

作者： Wei Zhang Chengchao Xu Jichao Sun Han-Ming Shen Jigang Wang Chuanbin Yang Department of Geriatrics Shenzhen People’s Hospital(the Second Clinical Medical CollegeJinan Universitythe First Affiliated HospitalSouthern University of Science and Technology)Shenzhen 518020China Integrated Chinese and Western Medicine Postdoctoral Research Station Jinan UniversityGuangzhou 510632China Artemisinin Research Center Institute of Chinese Materia MedicaChina Academy of Chinese Medical SciencesBeijing 100700China Faculty of Health Sciences University of MacaoTaipaMacao 999078China Guangdong Provincial Key Laboratory of New Drug Screening School of Pharmaceutical SciencesSouthern Medical UniversityGuangzhou 510515China

Alzheimer’s disease(AD),the most common neurodegenerative disorder,is characterized by memory loss and cognitive dysfunction.The accumulation of misfolded protein aggregates including amyloid beta(Aβ)peptides and microtubule associated protein tau(MAPT/tau)in neuronal cells are hallmarks of AD.So far,the exact underlying mechanisms for the aetiologies of AD have not been fully understood and the effective treatment for AD is limited.autophagy is an evolutionarily conserved cellular catabolic process by which damaged cellular organelles and protein aggregates are degraded via lysosomes.Recently,there is accumulating evidence linking the impairment of the autophagy-lysosomal pathway with AD pathogenesis.Interestingly,the enhancement of autophagy to remove protein aggregates has been proposed as a promising therapeutic strategy for AD.Here,we first summarize the recent genetic,pathological and experimental studies regarding the impairment of the autophagy-lysosomal pathway in AD.We then describe the interplay between the autophagy-lysosomal pathway and two pathological proteins,Aβand MAPT/tau,in AD.Finally,we discuss potential therapeutic strategies and small molecules that target the autophagy-lysosomal pathway for AD treatment both in animal models and in clinical trials.Overall,this article highlights the pivotal functions of the autophagy-lysosomal pathway in AD pathogenesis and potential druggable targets in the autophagy-lysosomal pathway for AD treatment.

关键词： Alzheimer’s disease(AD) Amyloid beta(Aβ)peptides MAPT/tau autophagy-lysosomal pathway autophagy enhancers autophagy Mitophagy Neurodegenerative diseases

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Recent developments of neuroprotective agents for degenerative retinal disorders

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Neural Regeneration Research 2022年第9期17卷 1919-1928页

作者： Kepeng Ou Youjian Li Ling Liu Hua Li Katherine Cox Jiahui Wu Jian Liu Andrew D.Dick College of Pharmacy National&Local Joint Engineering Research Center of Targeted and Innovative TherapeuticsIATTIChongqing University of Arts and SciencesChongqingChina Translational Health Sciences Bristol Medical SchoolUniversity of BristolBristolUK Department of Ophthalmology Yongchuan HospitalChongqing Medical UniversityChongqingChina Department of Ophthalmology Shanghai General Hospital(Shanghai First People’s Hospital)Shanghai Jiao Tong University School of MedicineShanghaiChina Institute of Ophthalmology University College LondonLondonUK National Institute for Health Research Biomedical Research Centre Moorfields Eye HospitalLondonUK

Retinal degeneration is a debilitating ocular complication characterized by the progressive loss of photoreceptors and other retinal neurons,which are caused by a group of retinal diseases affecting various age groups,and increasingly prevalent in the elderly.Age-related macular degeneration,diabetic retinopathy and glaucoma are among the most common complex degenerative retinal disorders,posing significant public health problems worldwide largely due to the aging society and the lack of effective therapeutics.Whilst pathoetiologies vary,if left untreated,loss of retinal neurons can result in an acquired degeneration and ultimately severe visual impairment.Irrespective of underlined etiology,loss of neurons and supporting cells including retinal pigment epithelium,microvascular endothelium,and glia,converges as the common endpoint of retinal degeneration and therefore discovery or repurposing of therapies to protect retinal neurons directly or indirectly are under intensive investigation.This review overviews recent developments of potential neuroprotectants including neuropeptides,exosomes,mitochondrial-derived peptides,complement inhibitors,senolytics,autophagy enhancers and antioxidants either still experimentally or in clinical trials.Effective treatments that possess direct or indirect neuroprotective properties would significantly lift the burden of visual handicap.

关键词： antioxidants autophagy enhancers complement inhibitors exosomes neuropeptides neuroprotective agents retinal degeneration senolytics

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