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Methylselenic acid (MSeA) has been observed to augment caspase-mediated apoptosis by down-regulating the expression of survivin, Bcl-xL, and Mcl-1, which are proteins that typically inhibit apoptosis (144, 145)

Importantly, NRN1-mediated axonal growth is neuron-type specific: it promotes outgrowth in projection neurons but does not affect interneurons (Nedivi et al., 1998)

It transitions from being primarily an energy-yielding pathway into a dynamic biosynthetic factory, redirecting carbon flux to support the massive demand for macromolecular synthesis - such as fatty acids, non-essential amino acids, and nucleotides - required for rapid proliferation

Moore et al., 2000), and similarly showed to induce ASD-like behaviors in mice and rats (Rodier et al., 1997