Adolfo Toledano-Díaz

This study aimed to determine luteinizing hormone preovulatory release, follicular dynamics, and ovulation in Arbia breed goats. Estrus was induced during the non-breeding season using progesterone, pregnant mare serum gonadotropin, and prostaglandin. Blood samples and ovarian transrectal ultrasound scanning were performed to determine luteinizing hormone concentrations, follicular growth, and ovulation. Luteinizing hormone values ranged between 0.00 and 3.85 ng mL-1. The average preovulatory luteinizing hormone peak was 2.40 Å} 1.39 ng mL-1 approximately at 27.81 Å} 4.19 hours after sponge removal. All females showed a preovulatory luteinizing hormone peak, with 81.82% of them between 24 and 30 hours after sponge removal. According to the ultrasonographic studies, the total mean follicular diameter ranged from 4.54 Å} 1.17 mm up to 11.6 Å} 0.56 mm at 0 and 48 hours after sponge removal, respectively. However, ovulation occurred between 30 and 36 hours after the hormonal induction protocol in 9 goats (81.8%), observing a mean preovulatory follicular diameter of 9.51 Å} 0.93 mm. The interval between the preovulatory luteinizing hormone peak and ovulation was 9.27 Å} 5.60 hours. It is concluded that preovulatory luteinizing hormone peak in Arbia goats occurred as early as 24–30 hours after sponge removal. Surprisingly, the interval between the luteinizing hormone peak and ovulation was shorter (9 hours) than that of the goat breeds studied so far, indicating that artificial insemination protocols should be specifically adjusted for this breed. Cite this article as: Amrane, A. A., Belhamiti, B. T., Selles, S. M. A., Kouidri, M., Chogueur, O., Díaz, A. T., Velázquez, R. G., & Moreno, J. S. (2026). The timing of the preovulatory luteinizing hormone surge, follicular dynamics and ovulation time observed with ultrasonography in Arbia goats. Acta Veterinaria Eurasia, 52, 0075, doi: 10.5152/actavet.2026.26075.

Background: Immunocontraception is a population management strategy based on vaccines that induce an immune response against reproductive targets such as GnRH. Objectives: This study aimed to investigate spermatogenic activity in adult baboons and adult dwarf bucks subject to repeated immunisation against GnRH for extended periods. Methods: In Experiment 1, histological findings in untreated dwarf bucks (CONTROL‐1) ( n =  10) were compared with those found in males repeatedly immunised against GnRH (Improvac) during 5 years (RI‐1; n =  15). In Experiment 2, one group of baboons received immunocontraceptive treatment against GnRH during 5–10 years until death (RI‑2; n =  6). The second group received the same treatment for 10 years before discontinuation, with the interval between treatment withdrawal and death ranging from 10 to 27 months (RI‑2+S; n =  19). As in Experiment 1, testicular tissue was collected post‐mortem and processed histologically. Results: In both species, the testicular tissue of animals treated with repeated immunisation against GnRH showed an absence of active spermatogenesis. The mean seminiferous tubule diameter in bucks was smaller in the RI‐1 group than in the CONTROL‐1 group (108.69 ± 13.17 µm vs. 187.35 ± 14.38 µm; p  < 0.05). In baboons, morphometric analysis showed similar seminiferous tubule diameters in the RI‐2 (82.63 ± 4.47 µm) and RI‐2+S (79.23 ± 5.89 µm) groups. Conclusions: In bucks and in more than 70% of baboons, the severity of degenerative changes in the germinal epithelium suggests that long‐term repeated immunisation against GnRH may lead to irreversible infertility.

NANOG is a conserved regulator of epiblast identity and is essential for hypoblast development and embryo survival after the blastocyst stage in mice. However, its role during post-blastocyst development remains poorly understood in non-rodent mammals. Here, we investigated the function of NANOG during ovine embryogenesis using CRISPR/Cas9-mediated gene ablation. NANOG ablation did not affect blastocyst formation or the initial development of the epiblast. However, NANOG -deficient blastocysts contained significantly fewer SOX17+ hypoblast cells by day (D) 8, followed by reduced hypoblast migration during early post-hatching stages in D12 in vitro embryos. These defects were transient, as hypoblast development was comparable between NANOG -deficient and wild-type conceptuses during subsequent in vivo conceptus elongation from embryonic day (E) 11 onwards. In contrast, although extraembryonic membranes development and conceptus elongation proceeded normally, NANOG-deficient conceptuses lacked SOX2+ epiblast cells and failed to form an embryonic disc (ED) from E11 onwards. These findings demonstrate that NANOG is dispensable for hypoblast development but is required for epiblast maintenance and ED formation during conceptus elongation in sheep.

Frontotemporal lobar degeneration (FTD) and Alzheimer’s disease (AD) are proteinopathies characterized by the abnormal accumulation and aggregation of specific proteins like Aβ-42 deposits, p-tau accumulation, and abnormal cytosolic aggregation of TAR DNA-binding protein 43 (TDP-43) in FTD patients. Recently, the identification of neuroinflammatory mediators as predictors of cognitive decline has gained attention. We have compared several plasma biomarkers of cognitive impairment between AD and FTD patients using Enzyme-Linked Immunosorbent Assay (ELISA) (pg/mL), including CX3CR1 and soluble fractalkine (sFK, also termed CX3CL1), TDP-43, neurofilament light chain M (NfL M), p-tau217, and GFAP (glial fibrillary acidic protein). Chemokines are HIV-1 co-receptors that facilitate the spread of HIV-1 infection and induce apoptosis in the brain. Whilst these chemokines promote neuronal survival and regulate neuron-glia interactions, they also contribute to neurodegeneration. Fractalkine, also known as CX3CL1, is a delta chemokine that binds to its CX3CR1 chemokine receptor. As a membrane isoform, fractalkine can be released in a soluble form by damaged neurons under either inflammatory and/or excitotoxic conditions; since neuroinflammation contributes to neurodegeneration and dementia, we compared these CX3CR1/sFK delta chemokine levels in seropositive patients (with suppressed viral loads) and without neurodegeneration to age-matched controls. This was done in order to study whether inflammation could upregulate these chemokines in the absence of cognitive impairment. To our knowledge, this is the first study showing that increased plasma levels of CX3CR1 and soluble fractalkine could be associated with FTD pathology as compared to control subjects (without neurodegeneration). However, peripheral NfL M, GFAP, and p-tau217 levels did not differ between AD and FTD patients. Post-mortem analysis of human FTD brains revealed anatomical changes, including hippocampal involution and tau deposits. Given that soluble fractalkine can contribute to cognitive impairment while also exerting protective effects against brain insults, we did an additional (independent experiment) in cortical neurons in vitro under LPS-induced neurotoxicity. We confirmed that adding recombinant fractalkine for 24 h prevented lipopolysaccharide (LPS)-induced apoptosis in cortical neurons at 7 days in vitro (DIV); moreover, twenty-four hours after LPS treatment, sFK prevented neuronal apoptosis by decreasing caspase-3 activity and exerted neuroprotective effects against inflammation. Our findings suggest that fractalkine mitigates LPS-induced neuronal injury by limiting apoptosis and inflammatory responses. Furthermore, our findings suggest for the first time that elevated circulating sFK levels may indirectly be associated with FTD pathology as compared to healthy controls. However, sFK could also reflect compensatory protective responses to neuronal injury.

Alzheimer’s disease (AD) is a multifactorial neurodegenerative disorder characterized by amyloid-β (Aβ) and the accumulation of tau in the brain, which triggers robust innate immune responses. Growing evidence indicates that neuroinflammation contributes to AD progression by overactivating microglia through the release of cytokines and chemokines. In general, chemokines can disrupt neuronal communication and promote blood–brain barrier permeability. Peripheral immune cells are mobilized into the brain by a gradient of chemokines. These processes link peripheral immune responses with substantial T-cell infiltration into the CNS parenchyma, leptomeninges and cerebrospinal fluid of both AD mice and AD patients. This finding underscores the relevance of the adaptive immune system, particularly T and B cells, in AD neuropathology. T-cell infiltration into the brain can influence amyloid clearance through chemokine signalling. However, chemokines play a critical role in AD by either promoting or suppressing disease progression. The infiltration of peripheral T and B cells into the brain parenchyma can exacerbate neuronal loss, yet it may also exert neuroprotective effects. Despite the presence of CD4⁺ and CD8⁺ T cells in postmortem brains of AD patients, debate continues about their role in AD brains, in terms of whether they are protective or detrimental. Understanding the complex role of chemokines in controlling innate and adaptive immune responses by modulating neuron–glia interactions (involving astrocytes and microglia) may provide novel therapeutic approaches for AD. Targeting chemokine signalling or treating with drugs that can prevent the recruitment of immune cells may be promising strategies for treating AD neuropathology. Therapies that prevent the overactivation of T cells in the brain could lead to protective strategies against AD. In fact, regulatory T cells (Tregs) could delay the onset of cognitive symptoms, because they suppress inflammation and slow the accumulation of Aβ plaques and p-Tau in the brain. Complementary strategies, such as photobiomodulation, nanoparticle, and T-cell-based approaches, could mitigate AD progression in patients.

The capercaillie ( Tetrao urogallus ), a critically endangered species, faces significant challenges due to habitat loss and population decline. Assisted reproductive technologies, including semen preservation and artificial insemination (AI), are vital for conservation efforts. Although the results are controversial, it has been reported that antioxidants, such as catalase, play an important role in protecting against oxidative damage caused by reactive oxygen species during short‐ and long‐term sperm storage. This study evaluated the protective effects of catalase (200 IU/mL) on stored/frozen‐thawed capercaillie sperm. The possible protective or harmful effect of catalase on fertilizing ability was assessed after AI with fresh and stored semen. Results indicated that catalase had no significant effect on sperm motility, viability, or DNA integrity after liquid storage or freezing/thawing. Fertility rates decreased sharply after semen storage for 6 h at 5°C even in the presence of catalase. Catalase‐treated samples maintained similar fertility rates to controls. The study also provided the first evidence of sperm storage duration within female capercaillies, which lasted up to 21 days. These findings underscore the challenges of semen preservation in wild species and highlight the need for further exploration of alternative antioxidants to optimize storage media.

Frontotemporal lobar degeneration (FTD) is a proteinopathy that induces neuroinflammation and neurodegeneration; Alzheimer´s disease (AD) is characterized by Abeta-42 deposits, microglia overactivation, astroglial alterations and p-Tau accumulation. Identification of neuroinflammatory mediators as predictors of cognitive cognition have gained attention. We compared several biomarkers in plasma as predictors of cognitive impairment between AD and FTD patients (Nfl, p-Tau217, TDP-43 and CX3CR1 and soluble fractalkine levels) by ELISA (pg/ml) and age-matched controls (without cognitive impairment) or HIV-1 seropositive patients. To our knowledge, this is the first study showing that increased plasma CX3CR1 and soluble fractalkine predict cognitive impairment specifically in FTD. In addition, high plasma p-Tau 271 levels correlate with sFK levels and their mini mental scores in FTD. Thus, fractalkine and TDP-43 are exclusive biomarkers of cognitive impairment in FTD. However, Nfl, GFAP and p-Tau271 levels did not differ between AD or FTD patients. Anatomically, we observed hippocampal involution as well as Tau deposits in human FTD postmortem brains. On the other hand, neuroinflammation contributes to dementia; and chemokines as HIV-1 co-receptors facilitate spread of HIV-1 infection inducing apoptosis in the brain. On the other hand, chemokines promote neuronal survival and regulate neuron-glia interactions. Fractalkine is a delta chemokine (also termed CX3CL1), that binds to its CX3CR1 chemokine receptor, that as a membrane-isoform can be released as a soluble form by damaged neurons. We confirmed that fractalkine prevents LPS (an inflammation inductor)-induced apoptosis by decreasing caspase-3 activation in cortical neurons at 7 DIV LPS exposure. Thus, fractalkine may play a dual role: it is associated with cognitive impairment in both FTD and AD, yet it also exerts neuroprotective effects by reducing LPS-induced neuronal apoptosis at 7 DIV.