Masters thesis — Sister Nivedita University, 2025. Full text: https://archive.org/details/sgng.20150-investigating-the-effect-of-copper-cui-depletion-on-the-serotoner
It demonstrates differential susceptibility in a clean model — the same trace-element deficiency destroys one neuron population and leaves another untouched, mirroring how Menkes disease patients show selective neurodegeneration.
Depleting copper (CuI) with tetrathiomolybdate in C. elegans selectively destroys serotonergic HSN neurons — broken axonal extensions, degraded egg-laying from impaired serotonin release to the vulval muscles — while pharyngeal ADF/NSM neurons stay structurally and functionally intact.
Why it matters
It demonstrates differential susceptibility in a clean model — the same trace-element deficiency destroys one neuron population and leaves another untouched, mirroring how Menkes disease patients show selective neurodegeneration.
Use when: Vulnerability is cell-type specific — a toxin's damage map tells you more about the system's architecture than about the toxin itself.
