Reducing Nav1.6 expression attenuates the pathogenesis of Alzheimer's disease by suppressing BACE1 transcription.

Aberrant increases in neuronal network excitability may contribute to cognitive deficits in Alzheimer's disease (AD). However, the mechanisms underlying hyperexcitability of neurons are not fully understood. Voltage-gated sodium channels (VGSC or Nav), which are involved in the formation of excitable cell's action potential and can directly influence the excitability of neural networks, have been implicated in AD-related abnormal neuronal hyperactivity and higher incidence of spontaneous non-convulsive seizures.

NCAM regulates temporal specification of neural progenitor cells via profilin2 during corticogenesis.

The development of cerebral cortex requires spatially and temporally orchestrated proliferation, migration, and differentiation of neural progenitor cells (NPCs). The molecular mechanisms underlying cortical development are, however, not fully understood. The neural cell adhesion molecule (NCAM) has been suggested to play a role in corticogenesis.

Mitochondrial Dysfunction in Neural Injury.

Mitochondria are the double membrane organelles providing most of the energy for cells. In addition, mitochondria also play essential roles in various cellular biological processes such as calcium signaling, apoptosis, ROS generation, cell growth, and cell cycle. Mitochondrial dysfunction is observed in various neurological disorders which harbor acute and chronic neural injury such as neurodegenerative diseases and ischemia, hypoxia-induced brain injury.