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Domith, I.

Publications and source records attributed to Domith, I..

2 recordsLinked to original sources

Lysergic Acid Diethylamide extends lifespan in Caenorhabditis elegans

Aging is modulated by nutrient-sensing pathways that integrate metabolic and hormonal cues to regulate growth, stress resilience, and lifespan. Caloric restriction (CR), a well-established intervention, extends longevity in diverse species through modulation of conserved nutrient-sensing pathways, including TOR signaling. Lysergic acid diethylamide (LSD), a classic serotonergic psychedelic with emerging therapeutic applications, remains largely unexplored in the context of aging. Here, we show that LSD treatment significantly extends lifespan in Caenorhabditis elegans and reduces age-associated lipofuscin accumulation, suggesting delayed age-associated decline. LSD induces several phenotypes that overlap with those observed in some caloric restriction paradigms, including reduced reproductive output, decreased body size, and the absence of an additive effect in lifespan assay performed in dietary restriction model, without apparent decreasing in food intake. In addition, LSD treatment modulates lipid stores and other cellular readouts associated with nutrient-sensing physiology. Together, these findings suggest that LSD engages evolutionarily conserved pathways linked to longevity and identify this compound as a tool to investigate serotonergic control of aging biology.

neuroscience↗

LSD Modulates Proteins Involved in Cell Proteostasis, Energy Metabolism and Neuroplasticity in Human Brain Organoids

Proteomic analysis of human cerebral organoids may reveal how psychedelics regulate biological processes, shedding light on drug-induced changes in the brain. This study elucidates the proteomic alterations induced by lysergic acid diethylamide (LSD) in human cerebral organoids. By employing high-resolution mass spectrometry-based proteomics, we quantitatively analyzed the differential abundance of proteins in cerebral organoids exposed to LSD. Our findings indicate changes in proteostasis, energy metabolism, and neuroplasticity-related pathways. Specifically, LSD exposure led to alterations in protein synthesis, folding, autophagy, and proteasomal degradation, suggesting a complex interplay in the regulation of neural cell function. Additionally, we observed modulation in glycolysis and oxidative phosphorylation, crucial for cellular energy management and synaptic function. In support of the proteomic data, complementary experiments demonstrated LSDs potential to enhance neurite outgrowth in vitro, confirming its impact on neuroplasticity. Collectively, our results provide a comprehensive insight into the molecular mechanisms through which LSD may affect neuroplasticity and potentially contribute to therapeutic effects for neuropsychiatric disorders.

neuroscience↗