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• W2532699523 abstract "Patients affected by Alzheimer’s disease (AD) develop amyloid deposits and hyperphosphorylated Tau aggregates in their brains long before cognitive deficits and neuronal loss can be measured, and the precise mechanism and pathways connecting these pathologies to neuronal death remain elusive. Modulating such pathways would be an attractive therapeutic strategy to slow the progression of AD and preserve patients’ cognitive function. Activation of c-jun N-terminal kinase (JNK) pathway is a critical player in response to stress and injury in both CNS and PNS neurons, and in many experimental settings, is linked to neuronal death. Genetic studies in C. elegans, Drosophila, and Mice has demonstrated that the neuron-specific mixed lineage kinase member Dual Leucine Zipper kinase (DLK, Map3k12) is required for stress-induced JNK pathway activation in multiple contexts, such as axonal injury, excitotoxicity, and toxin-induced neurodegeneration, and suggest that DLK acts upstream of JNK as a damage sensor controlling neuronal response to acute axonal damage. However, DLK expression in AD, where degeneration occurs slowly over time, has not been studied. In the present study, we examined DLK, the activated form of JNK (pJNK), and the target of JNK, p-c-Jun, by immunofluorescence at varying time points in multiple models of AD (APP TTA, 5XFAD, rTg4510, p25/cdk5). In control brains, DLK is expressed exclusively in neurons throughout most brain regions with a predominant localization to axons. However, in all models examined, DLK expression changes early in the pathological process and accumulates in damaged and dystrophic structures prior to neuronal death. In amyloid-based models, DLK accumulates near many amyloid plaques, whereas in the tau-based models, DLK is mislocalized to damaged axonal structures. The markers downstream of DLK signaling, pJNK and p-c-Jun, are elevated at later time points, depending on the model. These data suggest that DLK might play a critical role in triggering neurodegeneration in a slowly progressing degenerative condition such as AD in addition to its well-known role regulating the acute neuronal stress response." @default.
• W2532699523 created "2016-10-28" @default.
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• W2532699523 date "2016-07-01" @default.
• W2532699523 modified "2023-10-16" @default.
• W2532699523 title "P2-112: Expression of the Stress Response Regulatory Protein Dual Leucine Zipper Kinase (DLK) During the Development of Neuropathology in Alzheimer’s Disease" @default.
• W2532699523 doi "https://doi.org/10.1016/j.jalz.2016.06.1482" @default.
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