The impact of JNK on neuronal migration.
Level 5 - mechanism / opinion, no new human data
Narrative review synthesizing preclinical mechanistic and animal model research.
PubMed 24243099 · doi:10.1007/978-94-007-7687-6_3
What was done
The authors reviewed literature on the role of the c-Jun N-terminal kinase (JNK) signaling cascade in neuronal migration during cortical development. The review details the basic biochemistry of JNK pathway components, upstream regulators, downstream targets, phosphorylation of brain-specific proteins involved in microtubule homeostasis, and findings from transgenic mouse studies.
What was found
The abstract reports no experimental numbers or statistical effect sizes, noting only the baseline developmental rate that the fetal brain produces up to 250,000 cells per minute. It describes qualitative findings that JNK signaling cascade components and substrates regulate the speed, trajectory, and final positioning of migrating neurons in the cerebral cortex through modulation of microtubule homeostasis.
Why it matters
Elucidating the intracellular mechanisms controlling neuronal motility provides insight into normal brain layer formation and the pathogenesis of neurodevelopmental disorders tied to cortical malpositioning, such as epilepsy, intellectual disability, schizophrenia, and dyslexia.
Limits
The paper is a non-systematic narrative review focused on preclinical and transgenic mouse models, offering no primary data or human clinical evidence. The abstract does not specify search criteria, study counts, or quantitative outcome measures.
Cited by
- supports Neurons are formed in the fetal brain at a rate of 250,000 per minute during pregnancy.