Microglia PTK2B/Pyk2 in the Pathogenesis of Alzheimer’s Disease

小胶质细胞 发病机制 神经科学 神经退行性变 神经炎症 疾病 生物 促炎细胞因子 阿尔茨海默病 信号转导 医学 细胞生物学 病理 免疫学 炎症
作者
Yun Guo,Cheng-Kun Sun,Lian Tang,Meng‐Shan Tan
出处
期刊:Current Alzheimer Research [Bentham Science]
卷期号:20 (10): 692-704 被引量:1
标识
DOI:10.2174/0115672050299004240129051655
摘要

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 PTK2B 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.
最长约 10秒,即可获得该文献文件

科研通智能强力驱动
Strongly Powered by AbleSci AI
更新
大幅提高文件上传限制,最高150M (2024-4-1)

科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
thy完成签到 ,获得积分10
刚刚
chem完成签到,获得积分20
1秒前
Orange应助songvv采纳,获得10
1秒前
3秒前
黛寒发布了新的文献求助10
3秒前
airsh发布了新的文献求助10
4秒前
4秒前
4秒前
Jasper应助蒙蒙采纳,获得10
5秒前
Jasper应助丹D采纳,获得10
6秒前
成就夜柳完成签到,获得积分10
7秒前
勤恳绝义发布了新的文献求助10
7秒前
10秒前
潇洒的诗桃应助赛赛采纳,获得20
10秒前
11秒前
airsh完成签到,获得积分20
12秒前
12秒前
12秒前
13秒前
14秒前
桐桐应助臭皮匠1号采纳,获得10
14秒前
outman发布了新的文献求助30
15秒前
Xieyusen发布了新的文献求助10
16秒前
顾矜应助狡猾的家伙采纳,获得10
16秒前
勤恳绝义完成签到,获得积分20
17秒前
123发布了新的文献求助10
17秒前
18秒前
18秒前
songvv发布了新的文献求助10
19秒前
20秒前
drizzling发布了新的文献求助10
20秒前
今后应助韭菜盒子采纳,获得10
21秒前
22秒前
科研通AI2S应助Passion采纳,获得10
23秒前
可爱的函函应助YJ888采纳,获得10
24秒前
mhl11应助我有一只猫采纳,获得20
24秒前
宇月幸成发布了新的文献求助10
24秒前
小乔发布了新的文献求助10
25秒前
feng完成签到,获得积分10
26秒前
27秒前
高分求助中
The late Devonian Standard Conodont Zonation 2000
Nickel superalloy market size, share, growth, trends, and forecast 2023-2030 2000
The Lali Section: An Excellent Reference Section for Upper - Devonian in South China 1500
Smart but Scattered: The Revolutionary Executive Skills Approach to Helping Kids Reach Their Potential (第二版) 1000
Very-high-order BVD Schemes Using β-variable THINC Method 830
Mantiden: Faszinierende Lauerjäger Faszinierende Lauerjäger 800
PraxisRatgeber: Mantiden: Faszinierende Lauerjäger 800
热门求助领域 (近24小时)
化学 医学 生物 材料科学 工程类 有机化学 生物化学 物理 内科学 纳米技术 计算机科学 化学工程 复合材料 基因 遗传学 催化作用 物理化学 免疫学 量子力学 细胞生物学
热门帖子
关注 科研通微信公众号,转发送积分 3247443
求助须知:如何正确求助?哪些是违规求助? 2890794
关于积分的说明 8264627
捐赠科研通 2559134
什么是DOI,文献DOI怎么找? 1387790
科研通“疑难数据库(出版商)”最低求助积分说明 650653
邀请新用户注册赠送积分活动 627384