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Basic Science and Pathogenesis.

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Summary
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Nitrative stress activates JNK, impairing brain-derived neurotrophic factor (BDNF) transport in basal forebrain cholinergic neurons (BFCNs). Inhibiting JNK prevents this deficit, suggesting a target for age-related cognitive decline and Alzheimer's disease.

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Aging Research

Background:

  • Basal forebrain cholinergic neurons (BFCNs) are crucial for learning and memory.
  • Degeneration of BFCNs and impaired brain-derived neurotrophic factor (BDNF) transport contribute to cognitive decline in aging and Alzheimer's disease (AD).
  • Nitrative stress in the aging brain may disrupt BDNF transport, but the underlying mechanisms are not fully understood.

Purpose of the Study:

  • To investigate whether nitrative stress-induced activation of c-Jun N-terminal kinase (JNK) contributes to deficits in BDNF retrograde axonal transport in BFCNs.
  • To determine if inhibiting JNK can prevent nitrative stress-induced impairment of BDNF transport.

Main Methods:

  • Primary rat BFCNs were cultured in microfluidic chambers for axonal isolation.
  • Neurons were treated with a peroxynitrite donor (SIN-1) to induce nitrative stress.
  • JNK activation was measured via immunocytochemistry, and BDNF transport was assessed using Quantum dot-labeled BDNF and live-cell fluorescence microscopy.

Main Results:

  • Treatment with SIN-1 significantly increased JNK activation and decreased BDNF axonal transport.
  • Co-administration of a JNK inhibitor (CC401) with SIN-1 prevented the reduction in BDNF transport caused by SIN-1.
  • These findings indicate that JNK activation mediates the inhibitory effects of nitrative stress on BDNF transport.

Conclusions:

  • Activation of JNK by peroxynitrite is a key mechanism linking nitrative stress to impaired BDNF transport in BFCNs.
  • This study highlights a potential pathway through which age-related nitrative stress contributes to BFCN degeneration and cognitive decline in AD.
  • Targeting JNK signaling may offer a therapeutic strategy to preserve BDNF transport and mitigate cognitive deficits.