Increased levels of cerebrospinal fluid JNK3 associated with amyloid pathology: links to cognitive decline
Author(s) -
Sarah Gourmaud,
Claire Paquet,
Julien Dumurgier,
Clarisse Pace,
Constantin Bouras,
Françoise Gray,
Jean Laplanche,
Éliane Meurs,
François MoutonLiger,
Jacques Hugon
Publication year - 2015
Publication title -
journal of psychiatry and neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.767
H-Index - 99
eISSN - 1488-2434
pISSN - 1180-4882
DOI - 10.1503/jpn.140062
Subject(s) - senile plaques , cerebrospinal fluid , cognitive decline , alzheimer's disease , pathology , neurodegeneration , disease , kinase , tauopathy , medicine , degenerative disease , endocrinology , biology , dementia , biochemistry
Alzheimer disease is characterized by cognitive decline, senile plaques of β-amyloid (Aβ) peptides, neurofibrillary tangles composed of hyperphosphorylated τ proteins and neuronal loss. Aβ and τ are useful markers in the cerebrospinal fluid (CSF). C-Jun N-terminal kinases (JNKs) are serine-threonine protein kinases activated by phosphorylation and involved in neuronal death.
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