Role of proline‐rich tyrosine kinase 2 (Pyk2) in the pathogenesis of Alzheimer’s Disease

2021 ◽  
Author(s):  
Rahul Kumar ◽  
Vishvanath Tiwari ◽  
Sharmistha Dey
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Tyrosine Kinase ◽  
Tyrosine Kinase 2

scholarly journals Neuropathological characterization of Lemur tyrosine kinase 2 (LMTK2) in Alzheimer’s disease and neocortical Lewy body disease

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
János Bencze ◽  
Máté Szarka ◽  
Viktor Bencs ◽  
Renáta Nóra Szabó ◽  
Máté Smajda ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Tyrosine Kinase ◽  
Lewy Body ◽  
Lewy Body Disease ◽  
Cortical Layer ◽  
Cellular Processes ◽  
Tyrosine Kinase 2 ◽  
Post Mortem Brain ◽  
Significant Difference

AbstractAlzheimer’s disease (AD) and neocortical Lewy body disease (LBD) are the most common neurodegenerative dementias, with no available curative treatment. Elucidating pathomechanism and identifying novel therapeutic targets are of paramount importance. Lemur tyrosine kinase 2 (LMTK2) is involved in several physiological and pathological cellular processes. Herewith a neuropathological characterization is presented in AD and neocortical LBD samples using chromogenic and fluorescent LMTK2 immunohistochemistry on post-mortem brain tissues and compared them to age-matched controls (CNTs). LMTK2 immunopositivity was limited to the neuronal cytoplasm. Neurons, including tau-positive tangle-bearing ones, showed decreased chromogenic and immunofluorescent labelling in AD in every cortical layer compared to CNT and neocortical LBD. Digital image analysis was performed to measure the average immunopositivity of groups. Mean grey values were calculated for each group after measuring the grey scale LMTK2 signal intensity of each individual neuron. There was significant difference between the mean grey values of CNT vs. AD and neocortical LBD vs. AD. The moderate decrease in neocortical LBD suggests the effect of coexisting AD pathology. We provide neuropathological evidence on decreased neuronal LMTK2 immunolabelling in AD, with implications for pathogenesis.

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

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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