Biology subjects

Angeles Valdez, D.

Publications and source records attributed to Angeles Valdez, D..

3 recordsLinked to original sources

bioRxiv2025

First vs recurrent episode symptomatology in Major Depressive Disorder and its relation to brain function and structure: a network approach.

AbstractO_ST_ABSBackground.C_ST_ABSMajor Depressive Disorder (MDD) is a prevalent psychiatric disorder. At least half of the patients who recover from a first depressive episode, will experience a relapse. Therefore, understanding the underlying mechanisms supporting relapse is a clinical urgency that could be informed by studying complex brain-behavior associations. Here, we investigated how the relationships between depressive symptomatology and regional brain characteristics differed between people with first depressive episode vs recurrent depression. Methods.We used REST-meta-MDD data from the DIRECT consortium. We focused on comparing global and local network properties between first (n=239) and recurrent episode (n=179) on: (i) symptom network, (ii) brain structural (VBM) and functional networks (ALFF, ReHO), and (iii) integrated symptoms network and brain characteristics using the psychopathology and multimodal network approach. Results.Symptom network analysis showed high values of strength centrality for "Insomnia: Early Hours of the Morning" and "General somatic symptoms" at recurrence compared to the first episode. Also, differences in global strength in the integrated symptom-brain network (measured with ReHo metric) (S=2.09 p= 0.042). Finally, we found the edge of specific symptom-brain links, including insomnia and somatic symptoms-, to differ between the first episode and recurrence. Conclusions.For symptom networks, local but not global properties differentiated first from recurrent episode MDD, with specially stronger relations of insomnia and somatic symptoms in recurrent episode depression. For integrated symptom-brain networks, global strength of the network reflecting regional functional integrity (ReHO) was related to recurrence. This suggests that symptoms have relevance for understanding the complex brain-symptom relations underpinning recurrence of depression.

neuroscience↗

bioRxiv2025

Morphine self-administration induces region-specific brain volume changes and microglial phenotypic alterations without affecting neuronal density in male Wistar rats

Addiction to opioids, including morphine, is a major public health crisis in the U.S. It has been associated with brain volume changes in reward-related regions, neuronal death, and neuroinflammation. However, the link between structural changes and neuroinflammation is not well understood. In this study, we used operant conditioning to induce morphine self-administration in rats and examined brain volume and cellular changes, focusing on microglial phenotypes. Male Wistar rats were conditioned to morphine self-administration (0.01 mg/kg) for 20 days under a fixed-ratio 1 schedule. In vivo structural Magnetic Resonance Imaging (MRI) scans were conducted at the beginning and end of self-administration. Brains were stained for Iba1 and NeuN proteins, and confocal images were analyzed for cell counts and microglial morphology. We used Deformation-Based Morphometry for MRI volume analysis and Principal Component Analysis with K-means clustering for microglial phenotyping. Our results showed that morphine self-administration led to volume changes in addiction-related brain regions, including increased globus pallidus and decreased insular cortex volume. Additionally, morphine caused widespread neuroinflammation, evidenced by elevated microglial density in the caudate-putamen, dentate gyrus, globus pallidus, and insular cortex, without affecting neuron counts. Finally, we observed region-specific variations in microglial phenotypes, suggesting region-specific neuroinflammatory roles. In conclusion, our study shows that morphine self-administration induces structural and microglial changes in addiction-related brain regions without neuronal loss, highlighting the role of neuroinflammation in opioid-induced adaptations. The variability in microglial phenotypes underscores their complexity, emphasizing the need to study their progression in addiction and their potential as therapeutic targets.

neuroscience↗

bioRxiv2025

The effect of chronic stress and chronic alcohol intake on behavior, brain structure, and functional connectivity in a rat model

Pathological chronic stress is stress exceeding the organisms ability to cope physiologically, which may act as a risk factor in the onset and relapse of alcohol use disorder. Chronic- restraint stress (CRS) and ethanol intake are independently known to induce changes in brain structure and function, however, their combined effects on neurodevelopment over long periods of time remains largely unexplored. We conducted an in vivo longitudinal rat model with three main goals. 1) to determine if chronic stress increases ethanol intake; 2) to determine the effect of chronic- stress and ethanol intake in behavioral measures, brain structure, and function; and 3) to investigate the effect of sex. This observational study included Wistar rats assigned to four groups: 1) ethanol consumption (EtOH+/CRS-), 2) stress exposure (EtOH-/CRS+), 3) both ethanol and stress exposure (EtOH+/CRS+), and 4) control group (EtOH-/CRS-). Our results showed that chronic stress did not affect ethanol intake but led to reduced body weight gain, elevated corticosterone levels, and impaired recognition memory. Structural MRI revealed that both exposures produced additive brain volume changes in regions such as the olfactory bulb, orbitofrontal cortex, caudate-putamen, hippocampus, and cerebellum. Functional connectivity analysis using network-based statistics identified disrupted cortical-subcortical connections. Results found here were sex-dependent in terms of volumetric changes (higher effects on males) and functional connectivity (higher effects on females). Findings suggest sex-dependent mechanisms where both chronic- ethanol intake and stress affect brain plasticity during neurodevelopment. Understanding these region-specific vulnerabilities is crucial for addressing alcohol use disorders and stress-related neuropathology. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=173 SRC="FIGDIR/small/638122v1_ufig1.gif" ALT="Figure 1"> View larger version (50K): org.highwire.dtl.DTLVardef@27094dorg.highwire.dtl.DTLVardef@d3b8faorg.highwire.dtl.DTLVardef@155deeorg.highwire.dtl.DTLVardef@c9bb7b_HPS_FORMAT_FIGEXP M_FIG O_FLOATNOGraphical abstractC_FLOATNO Created with bioRender C_FIG

neuroscience↗