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Improving Blood Monocyte Energy Metabolism Enhances Its Ability to Phagocytose Amyloid-βand Prevents Alzheimer’s Disease-Type Pathology and Cognitive Deficits

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Neuroscience Bulletin 2023年第12期39卷 1775-1788页

作者： Zhi-Hao Liu Yu-Di Bai Zhong-Yuan Yu Hui-Yun Li Jie Liu Cheng-Rong Tan Gui-Hua Zeng Yun-Feng Tu Pu-Yang Sun Yu-Juan Jia Jin-Cai He Yan-Jiang Wang Xian-Le Bu Department of Neurology The First Affiliated Hospital of Wenzhou Medical UniversityWenzhou325000China Department of Neurology and Centre for Clinical Neuroscience Daping HospitalThird Military Medical UniversityChongqing400042China Chongqing Key Laboratory of Ageing and Brain Diseases Chongqing400042China Institute of Brain and Intelligence Third Military Medical UniversityChongqing400042China State Key Laboratory of Trauma Burns and Combined InjuryThird Military Medical UniversityChongqing400042China Center for Excellence in Brain Science and Intelligence Technology Chinese Academy of SciencesShanghai201200China

Deficiencies in the clearance of peripheral amyloidβ(Aβ)play a crucial role in the progression of Alzheimer’s disease(AD).Previous studies have shown that the ability of blood monocytes to phagocytose Aβis decreased in AD.However,the exact mechanism of Aβclearance dysfunction in AD monocytes remains unclear.In the present study,we found that blood monocytes in AD mice exhibited decreases in energy metabolism,which was accompanied by cellular senescence,a senescence-associated secretory phenotype,and dysfunctional phagocytosis of Aβ.Improving energy metabolism rejuvenated monocytes and enhanced their ability to phagocytose Aβin vivo and in vitro.Moreover,enhancing blood monocyte Aβphagocytosis by improving energy metabolism alleviated brain Aβdeposition and neuroinflammation and eventually improved cognitive function in AD mice.This study reveals a new mechanism of impaired Aβphagocytosis in monocytes and provides evidence that restoring their energy metabolism may be a novel therapeutic strategy for AD.

关键词： Alzheimer's disease Aβclearance Monocyte Phagocytosis Energy metabolism

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The relationship between amyloid-beta and brain capillary endothelial cells in Alzheimer's disease

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Neural Regeneration Research 2022年第11期17卷 2355-2363页

作者： Yan-Li Zhang Juan Wang Zhi-Na Zhang Qiang Su Jun-Hong Guo Department of Neurology First Hospital of Shanxi Medical UniversityTaiyuanShanxi ProvinceChina Department of Neurology Sixth Hospital of Shanxi Medical University(General Hospital of Tisco)TaiyuanShanxi ProvinceChina School of Public Health Shanxi Medical UniversityTaiyuanShanxi ProvinceChina

Neurovascular dysfunction,as an integral part of Alzheimer's disease,may have an important influence on the onset and progression of chronic neurodegenerative processes.The bloodbrain barrier(BBB)pathway is one of the main pathways that mediates the clearance of amyloidbeta(Aβ)in the brain parenchyma.A large number of studies have shown that receptors and ATPbinding cassette transporte rs expressed on endothelial cells play an important role in Aβtransport across the BBB,but the specific mechanism is not clear.In this review,we summarize the possible mechanisms of Aβproduction and clearance,and in particular the relationship between Aβand brain capillary endothelial cells.Aβis produced by abnormal cleavage of the amyloid precursor protein via amyloidogenic processing under pathological conditions.Dys regulation of Aβclearance is considered to be the main reason for the massive accumulation of Aβin the brain parenchyma.Several pathways mediating Aβclearance from the brain into the periphery have been identified,including the BBB pathway,the blood-cerebros pinal fluid barrier and arachnoid granule pathway,and the lymphoidrelated pathway.Brain ca pilla ry endothelial cells are the key components of Aβclearance mediated by BBB.Receptors(such as LRP1,RAGE,and FcRn)and ATP-binding cassette transporters(such as P-gp,ABCA1,and ABCC1)expressed on endothelial cells play a critical role in Aβtranscytosis across the BBB.The toxic effects of Aβcan induce dysregulation of receptor and transpo rter expression on endothelial cells.Excessive Aβexerts potent detrimental cerebrovascular effects by promoting oxidative stress,inducing chronic inflammation,and impairing endothelial structure and functions.All of these are main causes for the reduction in Aβclearance across the BBB and the accumulation of Aβin the brain parenchyma.Therefo re,studies on the intera ctions between Aβand brain capillary endothelial cells,including their receptors and transporters,studies on inhibition of the toxic effects of Aβon endothelial cells,and stud

关键词： Alzheimer's disease amyloid beta Aβclearance blood-brain barrier cerebral amyloid angiopathy dementia endothelial cells oxidative stress review therapeutics transcytosis

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