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DMT and Neuroprotection via the Sigma-1 Receptor DMT (N,N-dimethyltryptamine) activates the sigma-1 receptor (σ1R), an intracellular chaperone concentrated at mitochondria-associated endoplasmic reticulum membranes (MAMs). These contact sites regulate calcium signaling, energy production, and cellular stress responses. When σ1R is engaged, it helps stabilize the system under conditions that would otherwise damage or kill neurons and glia. Most of the clear protective data come from exogenous DMT, which reaches concentrations sufficient for robust receptor activation. Endogenous levels are typically much lower, so any natural contribution is likely subtler and more localized. Key findings include: • Hypoxia resistance — In human iPSC-derived cortical neurons and immune cells, DMT significantly increased survival under severe oxygen deprivation. Protection was abolished by σ1R knockdown or antagonism and linked to reduced HIF-1α activity (Szabo et al., 2016). • Ischemia and stroke models — Exogenous DMT reduced infarct volume, improved motor recovery, limited apoptotic and ferroptotic cell death, supported astrocytes, and shifted cytokine profiles toward anti-inflammatory patterns. Effects were blocked by selective σ1R antagonists (Nardai et al., 2020; Szabó et al., 2021). • Adult neurogenesis — DMT stimulated neural stem cell proliferation, neuroblast migration, and generation of new neurons in the hippocampal subgranular zone. Memory performance improved in treated animals. These effects depended on σ1R rather than classic serotonin receptors (Morales-Garcia et al., 2020). • Neurodegenerative models — In Alzheimer’s mouse models, chronic DMT improved cognition, reduced amyloid accumulation, restored σ1R levels, and normalized ER–mitochondria communication and mitochondrial function. Collectively, these studies indicate that σ1R activation by DMT supports neuronal and glial resilience through improved bioenergetics, reduced programmed cell death, lower inflammation, and enhanced plasticity. While the preclinical evidence is consistent, translation to clinical applications still requires careful evaluation of dosing, timing, and safety.