Role of a EphA‐4 receptor tyrosine kinase in the pathogenesis of Alzheimer’s Disease

2022 ◽  
Author(s):  
Devargya Ganguly ◽  
Joshua Abby Thomas ◽  
Abid Ali ◽  
Rahul Kumar
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Tyrosine Kinase ◽  
Receptor Tyrosine Kinase

scholarly journals Receptor tyrosine kinase ROR1 ameliorates Aβ1–42 induced cytoskeletal instability and is regulated by the miR146a-NEAT1 nexus in Alzheimer’s disease

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Kaushik Chanda ◽  
Nihar Ranjan Jana ◽  
Debashis Mukhopadhyay
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Tyrosine Kinase ◽  
Receptor Tyrosine Kinase ◽  
Cell Model ◽  
Actin Dynamics ◽  
Physical Interaction ◽  
Over Expression ◽  
Microtubule Disruption ◽  
Rna Immunoprecipitation

AbstractAlzheimer’s disease (AD) involves severe cytoskeletal degradation and microtubule disruption. Here, we studied the altered dynamics of ROR1, a Receptor Tyrosine Kinase (RTK), and how it could counter these abnormalities. We found that in an Aβ1–42 treated cell model of AD, ROR1 was significantly decreased. Over expressed ROR1 led to the abrogation of cytoskeletal protein degradation, even in the presence of Aβ1–42, preserved the actin network, altered actin dynamics and promoted neuritogenesis. Bioinformatically predicted miRNAs hsa-miR-146a and 34a were strongly up regulated in the cell model and their over expression repressed ROR1. LncRNA NEAT1, an interactor of these miRNAs, was elevated in mice AD brain and cell model concordantly. RNA Immunoprecipitation confirmed a physical interaction between the miRNAs and NEAT1. Intuitively, a transient knock down of NEAT1 increased their levels. To our knowledge, this is the first instance which implicates ROR1 in AD and proposes its role in preserving the cytoskeleton. The signalling modalities are uniquely analyzed from the regulatory perspectives with miR-146a and miR-34a repressing ROR1 and in turn getting regulated by NEAT1.

scholarly journals An isoform-specific role of FynT tyrosine kinase in Alzheimer's disease

2015 ◽  
Vol 136 (3) ◽  
pp. 637-650 ◽  
Author(s):  
Chingli Lee ◽  
Clara Y. B. Low ◽  
Paul T. Francis ◽  
Johannes Attems ◽  
Peter T.-H. Wong ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Tyrosine Kinase ◽  
Specific Role

P4-028: The role of fynt tyrosine kinase in astrocytes pertaining to neuroinflammation in Alzheimer's disease

2015 ◽  
Vol 11 (7S_Part_17) ◽  
pp. P776-P776
Author(s):  
Chingli Lee ◽  
Doris Xiu Wei Tan ◽  
Clara Ying Bei Low ◽  
Mitchell Kim Peng Lai ◽  
Michelle Guet Khim Tan
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Tyrosine Kinase

scholarly journals Hepatocyte Growth Factor in Synaptic Plasticity and Alzheimer's Disease

2010 ◽  
Vol 10 ◽  
pp. 457-461 ◽  
Author(s):  
Shiv K. Sharma
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Synaptic Plasticity ◽  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Receptor Tyrosine Kinase ◽  
Hippocampal Neurons ◽  
Different Types ◽  
Hepatocyte Growth

The hepatocyte growth factor (HGF) was initially identified as a protein that promoted growth of hepatocytes. It regulates proliferation and survival of different types of cells. HGF signaling, which is initiated by its binding to a receptor tyrosine kinase, plays critical roles during development. HGF and its receptor are also present in brain cells. This review describes the role of HGF in hippocampal neurons, synaptic plasticity, and the memory impairment condition, Alzheimer's disease.

Dissecting the role of Corticotropin-releasing hormone receptor type 1 in Alzheimer's Disease

2011 ◽  
Vol 44 (06) ◽  
Author(s):  
K Lerche ◽  
M Willem ◽  
K Kleinknecht ◽  
C Romberg ◽  
U Konietzko ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Hormone Receptor ◽  
Receptor Type ◽  
Corticotropin Releasing Hormone ◽  
Releasing Hormone

Role of melatonin in regulating neurogenesis: Implications for the neurodegenerative pathology and analogous therapeutics for Alzheimer’s disease

2020 ◽  
Vol 3 (2) ◽  
pp. 216-242 ◽  
Author(s):  
Mayuri Shukla ◽  
Areechun Sotthibundhu ◽  
Piyarat Govitrapong
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Adult Neurogenesis ◽  
Adult Brain ◽  
Therapeutic Approaches ◽  
Therapeutic Implications ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Differentiation ◽  
Progenitor Cell Proliferation

The revelation of adult brain exhibiting neurogenesis has established that the brain possesses great plasticity and that neurons could be spawned in the neurogenic zones where hippocampal adult neurogenesis attributes to learning and memory processes. With strong implications in brain functional homeostasis, aging and cognition, various aspects of adult neurogenesis reveal exuberant mechanistic associations thereby further aiding in facilitating the therapeutic approaches regarding the development of neurodegenerative processes in Alzheimer’s Disease (AD). Impaired neurogenesis has been significantly evident in AD with compromised hippocampal function and cognitive deficits. Melatonin the pineal indolamine augments neurogenesis and has been linked to AD development as its levels are compromised with disease progression. Here, in this review, we discuss and appraise the mechanisms via which melatonin regulates neurogenesis in pathophysiological conditions which would unravel the molecular basis in such conditions and its role in endogenous brain repair. Also, its components as key regulators of neural stem and progenitor cell proliferation and differentiation in the embryonic and adult brain would aid in accentuating the therapeutic implications of this indoleamine in line of prevention and treatment of AD.   

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