Current Alzheimer research最新文献_第9页

Microglia PTK2B/Pyk2 in the Pathogenesis of Alzheimer's Disease. 阿尔茨海默病发病机制中的小胶质细胞 PTK2B/Pyk2

Current Alzheimer research Pub Date : 2023-01-01 DOI: 10.2174/0115672050299004240129051655

Yun Guo, Cheng-Kun Sun, Lian Tang, Meng-Shan Tan

{"title":"Microglia PTK2B/Pyk2 in the Pathogenesis of Alzheimer's Disease.","authors":"Yun Guo, Cheng-Kun Sun, Lian Tang, Meng-Shan Tan","doi":"10.2174/0115672050299004240129051655","DOIUrl":"10.2174/0115672050299004240129051655","url":null,"abstract":"Alzheimer's disease (AD) is a highly hereditary disease with complex genetic susceptibility factors. Extensive genome-wide association studies have established a distinct susceptibility link between the protein tyrosine kinase 2β (PTK2B) gene and late-onset Alzheimer's disease (LOAD), but the specific pathogenic mechanisms remain incompletely understood. PTK2B is known to be expressed in neurons, and recent research has revealed its more important significance in microglia. Elucidating the role of PTK2B high expression in microglia in AD's progression is crucial for uncovering novel pathogenic mechanisms of the disease. Our review of existing studies suggests a close relationship between PTK2B/proline-rich tyrosine kinase 2 (Pyk2) and tau pathology, and this process might be β-amyloid (Aβ) dependence. Pyk2 is hypothesized as a pivotal target linking Aβ and tau pathologies. Concurrently, Aβ-activated Pyk2 participates in the regulation of microglial activation and its proinflammatory functions. Consequently, it is reasonable to presume that Pyk2 in microglia contributes to amyloid-induced tau pathology in AD via a neuroinflammatory pathway. Furthermore, many things remain unclear, such as identifying the specific pathways that lead to the release of downstream inflammatory factors due to Pyk2 phosphorylation and whether all types of inflammatory factors can activate neuronal kinase pathways. Additionally, further in vivo experiments are essential to validate this hypothesized pathway. Considering PTK2B/Pyk2's potential role in AD pathogenesis, targeting this pathway may offer innovative and promising therapeutic approaches for AD.","PeriodicalId":94309,"journal":{"name":"Current Alzheimer research","volume":" ","pages":"692-704"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139699223","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Antipsychotics in Alzheimer's Disease: Current Status and Therapeutic Alternatives. 阿尔茨海默病中的抗精神病药物：抗精神病药物在阿尔茨海默病中的应用：现状与治疗替代方案》（Current Status and Therapeutic Alternatives.

Current Alzheimer research Pub Date : 2023-01-01 DOI: 10.2174/0115672050287534240215052417

Maria Paula Maziero, Natalia P Rocha, Antonio L Teixeira

引用次数: 0

Accuracy of Telephone-Based Cognitive Screening Tests: Systematic Review and Meta-Analysis 基于电话的认知筛选测试的准确性：系统回顾与元分析

Current Alzheimer research Pub Date : 2020-04-01 DOI: 10.2174/15672050mta3qnjgj4

E. Elliott

引用次数: 6

Withdrawn: Biomarkers in Alzheimer's Disease-Recent Update. 撤回：阿尔茨海默病的生物标志物--近期更新。

Current Alzheimer research Pub Date : 2017-02-20

引用次数: 0

PERK-opathies: An Endoplasmic Reticulum Stress Mechanism Underlying Neurodegeneration. PERK病：神经变性的内质网应激机制。

Current Alzheimer research Pub Date : 2016-01-01 DOI: 10.2174/1567205013666151218145431

Michelle C Bell, Shelby E Meier, Alexandria L Ingram, Jose F Abisambra

{"title":"PERK-opathies: An Endoplasmic Reticulum Stress Mechanism Underlying Neurodegeneration.","authors":"Michelle C Bell, Shelby E Meier, Alexandria L Ingram, Jose F Abisambra","doi":"10.2174/1567205013666151218145431","DOIUrl":"https://doi.org/10.2174/1567205013666151218145431","url":null,"abstract":"The unfolded protein response (UPR) plays a vital role in maintaining cell homeostasis as a consequence of endoplasmic reticulum (ER) stress. However, prolonged UPR activity leads to cell death. This time-dependent dual functionality of the UPR represents the adaptive and cytotoxic pathways that result from ER stress. Chronic UPR activation in systemic and neurodegenerative diseases has been identified as an early sign of cellular dyshomeostasis. The Protein Kinase R-like ER Kinase (PERK) pathway is one of three major branches in the UPR, and it is the only one to modulate protein synthesis as an adaptive response. The specific identification of prolonged PERK activity has been correlated with the progression of disorders such as diabetes, Alzheimer's disease, and cancer, suggesting that PERK plays a role in the pathology of these disorders. For the first time, the term \"PERK-opathies\" is used to group these diseases in which PERK mediates detriment to the cell culminating in chronic disorders. This article reviews the literature documenting links between systemic disorders with the UPR, but with a specific emphasis on the PERK pathway. Then, articles reporting links between the UPR, and more specifically PERK, and neurodegenerative disorders are presented. Finally, a therapeutic perspective is discussed, where PERK interventions could be potential remedies for cellular dysfunction in chronic neurodegenerative disorders. ","PeriodicalId":94309,"journal":{"name":"Current Alzheimer research","volume":"13 2","pages":"150-63"},"PeriodicalIF":0.0,"publicationDate":"2016-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6542591/pdf/nihms-1025111.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41224631","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 54