Hypothesis: JNK signaling is a therapeutic target of neurodegenerative diseases

Result code in IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F62690094%3A18470%2F22%3A50018093" target="_blank" >RIV/62690094:18470/22:50018093 - isvavai.cz</a>

Result on the web

<a href="https://alz-journals.onlinelibrary.wiley.com/doi/abs/10.1002/alz.12370" target="_blank" >https://alz-journals.onlinelibrary.wiley.com/doi/abs/10.1002/alz.12370</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1002/alz.12370" target="_blank" >10.1002/alz.12370</a>

Result language

angličtina

Original language name

Hypothesis: JNK signaling is a therapeutic target of neurodegenerative diseases

Original language description

The exact signaling leading to neurological dysfunction in neurodegenerative diseases is currently unknown. We hypothesize that the c-Jun N-terminal kinase (JNK) signaling pathway is a potential therapeutic target for neurodegenerative diseases. This postulate rests on extensive data from cell and animal experimental studies, demonstrating that JNK signaling plays a crucial role in the pathogenesis of neurodegenerative diseases. The sustained activation of JNK leads to synaptic dysfunction and even neuronal apoptosis, ultimately resulting in memory deficits and neurodegeneration. JNK phosphorylates the amyloid precursor protein and tau, ultimately resulting in the formation of extraneuronal senile plaques and intraneuronal neurofibrillary tangles. Our hypothesis could be validated by investigating the cerebral cortex of elderly chimpanzees injected with phosphorylated JNK or transgenic pig and chimpanzee models established using gene editing technology including CRISPR. This hypothesis provides clues for further understanding the molecular mechanisms of neurodegenerative diseases and the development of potential target therapeutic drugs.

Czech name

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Czech description

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Type

J_imp - Article in a specialist periodical, which is included in the Web of Science database

CEP classification

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OECD FORD branch

30210 - Clinical neurology

Project

—

Continuities

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Publication year

2022

Confidentiality

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Name of the periodical

ALZHEIMERS &amp; DEMENTIA

ISSN

1552-5260

e-ISSN

1552-5279

Volume of the periodical

18

Issue of the periodical within the volume

1

Country of publishing house

US - UNITED STATES

Number of pages

7

Pages from-to

152-158

UT code for WoS article

000655139000001

EID of the result in the Scopus database

2-s2.0-85106246435