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It is becoming increasingly evident that Artificial intelligence (AI) development draws inspiration from the architecture and functions of the human brain. This manuscript examines the alignment between key brain regions—such as the brainstem, sensory cortices, basal ganglia, thalamus, limbic system, and prefrontal cortex—and AI paradigms, including generic AI, machine learning, deep learning, and artificial general intelligence (AGI). By mapping these neural and computational architectures, I herein highlight how AI models progressively mimic the brain’s complexity, from basic pattern recognition and association to advanced reasoning. Current challenges, such as overcoming learning limitations and achieving comparable neuroplasticity, are addressed alongside emerging innovations like neuromorphic computing. Given the rapid pace of AI advancements in recent years, this work underscores the importance of continuously reassessing our understanding as technology evolves exponentially.

Embryonic development represents a highly coordinated biological continuum, beginning at fertilization and extending through fetal life to birth [...].Embryonic development represents a highly coordinated biological continuum, beginning at fertilization and extending through fetal life to birth [...].

Infertility is a global phenomenon that impacts people of both the male and the female sex; it is related to multiple factors affecting an individual’s overall systemic health. Recently, investigators have been using mesenchymal stem cell (MSC) therapy for female-fertility-related disorders such as polycystic ovarian syndrome (PCOS), premature ovarian failure (POF), endometriosis, preeclampsia, and Asherman syndrome (AS). Studies have shown promising results, indicating that MSCs can enhance ovarian function and restore fertility for affected individuals. Due to their regenerative effects and their participation in several paracrine pathways, MSCs can improve the fertility outcome. However, their beneficial effects are dependent on the methodologies and materials used from isolation to reimplantation. In this review, we provide an overview of the protocols and methods used in applications of MSCs. Moreover, we summarize the findings of published preclinical studies on infertility treatments and discuss the multiple properties of these studies, depending on the isolation source of the MSCs used.

Motor neuron diseases (MNDs) are a heterogeneous group of neurodegenerative disorders characterized by the progressive loss of motor neurons, resulting in debilitating physical decline. Advances in genetics have revolutionized the understanding of MNDs, elucidating critical genes such as SOD1, TARDBP, FUS, and C9orf72, which are implicated in their pathogenesis. Despite these breakthroughs, significant gaps persist in understanding the interplay between genetic and environmental factors, the role of rare variants, and epigenetic contributions. This review synthesizes current knowledge on the genetic landscape of MNDs, highlights challenges in linking genotype to phenotype, and discusses the promise of precision medicine approaches. Emphasis is placed on emerging strategies, such as gene therapy and targeted molecular interventions, offering hope for personalized treatments. Addressing these challenges is imperative to harness the full potential of genomics for improving outcomes in MNDs.

We have previously reported evidence that Nogo-A activation of Nogo-receptor 1 (NgR1) can drive axonal dystrophy during the neurological progression of experimental autoimmune encephalomyelitis (EAE). However, the B-cell activating factor (BAFF/BlyS) may also be an important ligand of NgR during neuroinflammation. In the current study we define that NgR1 and its homologs may contribute to immune cell signaling during EAE. Meningeal B-cells expressing NgR1 and NgR3 were identified within the lumbosacral spinal cords of ngr1 +/+ EAE-induced mice at clinical score 1. Furthermore, increased secretion of immunoglobulins that bound to central nervous system myelin were shown to be generated from isolated NgR1- and NgR3-expressing B-cells of ngr1 +/+ EAE-induced mice. In vitro BAFF stimulation of NgR1- and NgR3-expressing B cells, directed them into the cell cycle DNA synthesis phase. However, when we antagonized BAFF signaling by co-incubation with recombinant BAFF-R, NgR1-Fc, or NgR3 peptides, the B cells remained in the G0/G1 phase. The data suggest that B cells express NgR1 and NgR3 during EAE, being localized to infiltrates of the meninges and that their regulation is governed by BAFF signaling.

Exercise training (ET) has demonstrated beneficial effects in autoimmune and neurological disorders, including multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis (EAE). ET modulates the gut microbiota, which influences neuroimmune interactions via the microbiota-gut-brain and microbiota-gut-immune system axes. However, the role of gut microbiota in mediating ET’s protective effects in autoimmune neuroinflammation remains unclear. We investigated whether gut microbiota mediates the beneficial effects of ET on EAE development. Healthy mice underwent high-intensity continuous training (HICT). Fecal microbiota from HICT and sedentary mice were transplanted into naïve recipients, followed by proteolipid protein (PLP) immunization to induce EAE. Disease severity, gut microbial composition (16S rDNA sequencing), short-chain fatty acid (SCFA) levels (LC–MS), and autoreactive T-cell proliferation (flow cytometry) were assessed. Faecal microbiota transplantation (FMT) from HICT donors significantly reduced EAE severity, delaying onset and decreasing CNS inflammation, demyelination, and axonal damage. These effects correlated with distinct microbial signatures, including increased Faecalimonas and Escherichia genera, and decreased Mucispirillum genus. HICT-FMT mice exhibited higher Faecalimonas abundance and reduced serum SCFA levels. PLP-reactive T-cell proliferation was suppressed in HICT-FMT recipients. Gut microbiota from HICT mice confers protection against EAE development, associated with microbial-metabolic shifts and modulation of autoreactive T-cell responses.

The secondary sex ratio (SSR), defined as the ratio of male to female live births in a population, is a crucial indicator of reproductive and public health. External factors, such as lifestyle, natural disasters, environmental chemicals and infections, have been examined as potential trendsetters of the SSR. Several global challenges have emerged in recent years, such as climate change, wars, terrorist attacks and stressful political events. These aspects can potentially impact reproductive health outcomes, fertility rates, and the overall well-being of individuals. With respect to this, they may also affect the SSR. Through an in-depth examination of the existing literature, this manuscript elucidates the complex interconnections between global challenges and the SSR. Indeed, terrorist attacks and stressful political events have been linked to a decrease in the SSR. In contrast, high temperatures and warfare have shown a propensity to elevate the SSR in numerous scenarios. However, these associations require further validation through additional studies. The precise mechanisms through which these determinants exert their influence need to be elucidated. Understanding the unseen influences of global challenges on the SSR is crucial for understanding population trends and ensuring effective public health interventions.

The secondary sex ratio (SSR), defined as the ratio of male to female births in a population, has long been a subject of scientific inquiry due to its potential as a health indicator. The interplay between catastrophic events and the delicate balance of male and female births presents a nuanced and compelling study area. Natural disasters, such as earthquakes, hurricanes, floods, and volcanic eruptions, have been known to disrupt ecosystems and human populations, leading to both short-term and long-term consequences. Studies have suggested a potential influence of these disasters on the SSR, with varying degrees of impact observed across different regions and disaster types. Similarly, nuclear accidents, such as the infamous Chernobyl disaster, have sparked interest in their potential effects on human health and development. The release of radioactive materials into the environment can have far-reaching consequences, including impacts on reproductive outcomes. Through a rigorous examination of the existing literature, the present review aims to synthesize current knowledge on the impacts of natural disasters and nuclear accidents on the SSR and unravel the mechanisms that explain SSR fluctuations. By shedding light on the diverse influences shaping the SSR, this narrative review contributes to a deeper appreciation of the intricate interplay between environmental, biological, and societal factors that determines the SSR, calling for targeted strategies to mitigate potential adverse effects on sex ratios in the aftermath of such events.

Multiple sclerosis (MS) can progress with neurodegeneration as a consequence of chronic inflammatory mechanisms that drive neural cell loss and/or neuroaxonal dystrophy in the central nervous system. Immune-mediated mechanisms can accumulate myelin debris in the disease extracellular milieu during chronic-active demyelination that can limit neurorepair/plasticity and experimental evidence suggests that potentiated removal of myelin debris can promote neurorepair in models of MS. The myelin-associated inhibitory factors (MAIFs) are integral contributors to neurodegenerative processes in models of trauma and experimental MS-like disease that can be targeted to promote neurorepair. This review highlights the molecular and cellular mechanisms that drive neurodegeneration as a consequence of chronic-active inflammation and outlines plausible therapeutic approaches to antagonize the MAIFs during the evolution of neuroinflammatory lesions. Moreover, investigative lines for translation of targeted therapies against these myelin inhibitors are defined with an emphasis on the chief MAIF, Nogo-A, that may demonstrate clinical efficacy of neurorepair during progressive MS.