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Geribaldi-Doldan, N.

Publications and source records attributed to Geribaldi-Doldan, N..

2 recordsLinked to original sources

Longitudinal proteomic module configurations differ across human monocyte-derived differentiation and polarization conditions

Human monocyte differentiation involves changes in multiple protein programs, but comparisons across culture conditions can conflate source variation with differentiation time. We reanalyzed public proteomic measurements arranged in four source blocks across M1-polarizing, M2-polarizing, dendritic-cell and osteoclast conditions at days 2, 4, 6, 8 and 10. The original experiment used three individual-donor preparations and one preparation pooled from 40 donors; these are not four individual donors. Eight predefined protein-module scores formed an 80-observation matrix. A multivariate model tested joint condition and condition-by-time terms beyond source block and categorical time, using 9,999 permutations that preserved complete block-specific culture trajectories. The joint condition terms accounted for an additional 31.37% of total module-score variation (pseudo-F = 4.257567; permutation p = 0.0002). The association persisted after omission of each source block, with incremental R-squared of 0.315-0.390. Secondary day-specific tests detected differences at days 4-10, whereas day 2 did not meet the false-discovery criterion. Descriptive trajectories showed a shared increase in glycolysis/pentose-phosphate scores alongside condition-dependent mitochondrial, redox and proteostasis profiles. At day 10, M2-labelled cultures had the lowest mean mitochondrial score, whereas M1-labelled cultures had the highest three-protein resolution-associated score. All eight module tests survived multiplicity correction, and no single-module omission abolished the multivariate association. These findings describe condition-associated configurations within four heterogeneous source preparations. Equal weighting of source blocks does not estimate a mean across individual donors. The analysis does not establish pathway activity, single-cell trajectories, population-level replication or external biological validation.

immunology↗

Rescue of neurogenesis and age-associated cognitive decline in SAMP8 mouse: role of transforming growth factor alpha

Neuropathological aging is associated with memory impairment and cognitive decline, and affects several brain areas including the neurogenic niche of the dentate gyrus of the hippocampus (DG). In the healthy brain homeostatic mechanisms regulate neurogenesis in the DG to facilitate the continuous generation of neurons from neural stem cells (NSC). Nevertheless, aging reduces the number of activated neural stem cells, and diminishes the number of newly generated neurons. Strategies that promote neurogenesis in the DG may improve cognitive performance in the elderly resulting in the development of treatments to prevent the progression of neurological disorders in the aged population. Our work is aimed to discover targeting molecules to be used in the design of pharmacological agents to prevent the neurological effects of pathological aging. We study the effect of age on hippocampal neurogenesis using the SAMP8 mouse as a model of pathological aging. Thus, we show that in six-month-old SAMP8 mice, episodic and spatial memory are impaired, concomitantly the generation of neuroblasts and neurons is reduced and the generation of astrocytes is increased in this model. The novelty of our work resides in the fact that treatment of SAMP8 mice with a TGF-alpha targeting molecule, prevents the observed defects, positively regulating neurogenesis and improving cognitive performance. This compound facilitates the release of TGF-alpha in vitro and in vivo and activates signaling pathways initiated by this growth factor. We conclude that targeting the release of TGF-alpha may be the basis of pharmacological drugs to counteract the neurological effects of pathological aging.

neuroscience↗