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Neurologic impairments are usually irreversible as a result of limited regeneration in the central nervous system. Therefore, based on the regenerative capacity of stem cells, transplantation therapies of various stem cells have been tested in basic research and preclinical trials, and some have shown great prospects. This manuscript overviews the cellular and molecular characteristics of embryonic stem cells, induced pluripotent stem cells, neural stem cells, retinal stem/progenitor cells, mesenchymal stem/stromal cells, and their derivatives in vivo and in vitro as sources for regenerative therapy. These cells have all been considered as candidates to treat several major neurological disorders and diseases, owing to their self-renewal capacity, multi-directional differentiation, neurotrophic properties, and immune modulation effects. We also review representative basic research and recent clinical trials using stem cells for neurodegenerative diseases, including Parkinson's disease, Alzheimer's disease, and age-related macular degeneration, as well as traumatic brain injury and glioblastoma. In spite of a few unsuccessful cases, risks of tumorigenicity, and ethical concerns, most results of animal experiments and clinical trials demonstrate efficacious therapeutic effects of stem cells in the treatment of nervous system disease. In summary, these emerging findings in regenerative medicine are likely to contribute to breakthroughs in the treatment of neurological disorders. Thus, stem cells are a promising candidate for the treatment of nervous system diseases.

Alzheimer's disease is a common progressive neurodegenerative disorder, pathologically characterized by the presence of β-amyloid plaques and neurofibrillary tangles. Current treatment approaches using drugs only alleviate the symptoms without curing the disease, which is a serious issue and influences the quality of life of the patients and their caregivers. In recent years, stem cell technology has provided new insights into the treatment of neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis. Currently, the main sources of stem cells include neural stem cells, embryonic stem cells, mesenchymal stem cells, and induced pluripotent stem cells. In this review, we discuss the pathophysiology and general treatment of Alzheimer's disease, and the current state of stem cell transplantation in the treatment of Alzheimer's disease. We also assess future challenges in the clinical application and drug development of stem cell transplantation as a treatment for Alzheimer's disease.

Cerebral ischemic injury is the main manifestation of stroke, and its incidence in stroke patients is 70-80%. Although ischemic stroke can be treated with tissue-type plasminogen activator, its time window of effectiveness is narrow. Therefore, the incidence of paralysis, hypoesthesia, aphasia, dysphagia, and cognitive impairment caused by cerebral ischemia is high. Nerve tissue regeneration can promote the recovery of the aforementioned dysfunction. Neural stem cells can participate in the reconstruction of the damaged nervous system and promote the recovery of nervous function during self-repair of damaged brain tissue. Neural stem cell transplantation for ischemic stroke has been a hot topic for more than 10 years. This review discusses the treatment of ischemic stroke with neural stem cells, as well as the mechanisms of their involvement in stroke treatment.

Opinion statement The discovery of adult cardiac stem cells (CSCs) and their potential to restore functional cardiac tissue has fueled unprecedented interest in recent years. Indeed, stem-cell–based therapies have the potential to transform the treatment and prognosis of heart failure, for they have the potential to eliminate the underlying cause of the disease by reconstituting the damaged heart with functional cardiac cells. Over the last decade, several independent laboratories have demonstrated the utility of c-kit+/Lin- resident CSCs in alleviating left ventricular dysfunction and remodeling in animal models of acute and chronic myocardial infarction. Recently, the first clinical trial of autologous CSCs for treatment of heart failure resulting from ischemic heart disease (Stem Cell Infusion in Patients with Ischemic cardiOmyopathy [SCIPIO]) has been conducted, and the interim results are quite promising. In this phase I trial, no adverse effects attributable to the CSC treatment have been noted, and CSC-treated patients showed a significant improvement in ejection fraction at 1 year (+13.7 absolute units versus baseline), accompanied by a 30.2 % reduction in infarct size. Moreover, the CSC-induced enhancement in cardiac structure and function was associated with a significant improvement in the New York Heart Association (NYHA) functional class and in the quality of life, as measured by the Minnesota Living with Heart failure Questionnaire. These results are exciting and warrant larger, phase II studies. However, CSC therapy for cardiac repair is still in its infancy, and many hurdles need to be overcome to further enhance the therapeutic efficacy of CSCs.

DNA damage repair is induced by several factors and is critical for cell survival, and many cellular DNA damage repair mechanisms are closely linked. Antioxidant enzymes that control cytokine-induced peroxide levels, such as peroxiredoxins (Prxs) and catalase (CAT), are involved in DNA repair systems. We previously demonstrated that placenta-derived mesenchymal stem cells (PD-MSCs) that overexpress PRL-1 (PRL-1(+)) promote liver regeneration via antioxidant effects in TAA-injured livers. However, the efficacy of these cells in regeneration and the role of Prxs in their DNA repair system have not been reported. Therefore, our objective was to analyze the Prx-based DNA repair mechanism in naïve or PRL-1(+)-transplanted TAA-injured rat livers. Apoptotic cell numbers were significantly decreased in the PRL-1(+) transplantation group versus the nontransplantation (NTx) group (p < 0.05). The expression of antioxidant markers was significantly increased in PRL-1(+) cells compared to NTx cells (p < 0.05). MitoSOX and Prx3 demonstrated a significant negative correlation coefficient (R2 = −0.8123). Furthermore, DNA damage marker levels were significantly decreased in PRL-1(+) cells compared to NTx cells (p < 0.05). In conclusion, increased Prx3 levels in PRL-1(+) cells result in an effective antioxidant effect in TAA-injured liver disease, and Prx3 is also involved in repairing damaged DNA.

Opinion statement Owing to the prevalence of heart disease and the lack of effective long-term solutions for managing cardiac injury, research has turned to cell therapy as a potential mechanism for myocardial repair. Mesenchymal stem cells (MSC) in particular have become popular because their differentiative ability and their angiogenic and immunomodulatory properties make them attractive candidates for transplantation. However, there is still debate regarding the optimal strategy for the delivery of these cells. Recent clinical studies have isolated MSCs from a variety of tissue origins and have also tested the benefits of pretreatment with cardiogenic growth factors. Meanwhile, a newer school of thought instead supports the utilization of cardiomyocytes generated from MSC-derived induced pluripotent stem cells. This review will examine the promise of MSC therapy, discuss the results of past work, and propose steps that must be taken in the future.

Opinion statement Stem cell therapy is a promising therapeutic option for severe cardiac diseases that are resistant to conventional therapies. To overcome the unsatisfactory results of most clinical researches on stem cell injections to an injured heart, we are developing bioengineered cardiac tissue grafts using pluripotent stem cell-derived cardiomyocytes and vascular cells. We have validated the functional benefits of mouse embryonic stem cell-derived and human induced pluripotent stem cell-derived cardiac tissue sheets (CTSs) in a rat myocardial infarction model. We further showed enhanced functional recovery and engraftment efficiency leading to de novo myocardium upon transplanting thick multi-layered CTSs that had gelatin hydrogel microspheres between the layers. We anticipate that the combination of pluripotent stem cell biology and tissue engineering will contribute to future stem cell therapies for severe heart diseases.

This study reports on 382 COVID-19 patients having undergone allogeneic ( n  = 236) or autologous ( n  = 146) hematopoietic cell transplantation (HCT) reported to the European Society for Blood and Marrow Transplantation (EBMT) or to the Spanish Group of Hematopoietic Stem Cell Transplantation (GETH). The median age was 54.1 years (1.0–80.3) for allogeneic, and 60.6 years (7.7–81.6) for autologous HCT patients. The median time from HCT to COVID-19 was 15.8 months (0.2–292.7) in allogeneic and 24.6 months (−0.9 to 350.3) in autologous recipients. 83.5% developed lower respiratory tract disease and 22.5% were admitted to an ICU. Overall survival at 6 weeks from diagnosis was 77.9% and 72.1% in allogeneic and autologous recipients, respectively. Children had a survival of 93.4%. In multivariate analysis, older age ( p  = 0.02), need for ICU ( p  < 0.0001) and moderate/high immunodeficiency index ( p  = 0.04) increased the risk while better performance status ( p  = 0.001) decreased the risk for mortality. Other factors such as underlying diagnosis, time from HCT, GVHD, or ongoing immunosuppression did not significantly impact overall survival. We conclude that HCT patients are at high risk of developing LRTD, require admission to ICU, and have increased mortality in COVID-19.

Ischemic stroke induces irreversible cerebral tissue damage, a condition exacerbated by the brain’s limited endogenous neuroplasticity and inability to regenerate neurons. While neural circuit reorganization holds therapeutic potential, its efficacy is hindered by pathological barriers such as glial scarring, chronic inflammation, and neurotrophic factor deficiency. Although pharmacological and interventional methods for stroke have been well developed, their functional recovery outcomes remain suboptimal. Emerging neural regeneration paradigms, particularly stem cell-based strategies (encompassing neural stem cell transplantation, neural progenitors grafts, and 3D brain organoid implantation), offer novel solutions to these challenges. However, critical limitations persist in conventional stem cell approaches: (1) compromised synaptic integration efficacy hinders functional neural circuit reconstruction; (2) the absence of functional vascular niches coupled with deficient astrocyte-mediated support and extracellular matrix signaling; (3) restricted regenerative capacity despite theoretical multipotent differentiation potential. Recent breakthroughs in cerebral organoid technology have revolutionized neurological disease modeling and neural repair research. Building upon this paradigm shift, our study mechanistically interrogates neuroplastic remodeling processes following ischemic stroke, while critically evaluating the therapeutic efficacy and inherent limitations of stem cell-based interventions. This affirms the critical role of 3D human cerebral organoid transplantation in the reconstruction of neural circuits. Additionally, we further summarize the utility of organoid-based disease models and address associated ethical and societal concerns. Future efforts should prioritize the clinical translation of organoid transplantation for ischemic stroke, aiming to mitigate neurological deficits and restore functional recovery.

The adult brain can produce only a relatively small number of new neurons, and neurogenesis occurs only in specific brain areas. Post-neuronal injury self-repair is very slow and sometimes does not occur. Therefore, advancements in regenerative therapies play an essential role in recovery from damage. This review focuses on stem cell-based neuronal repair by using biomaterials. We discuss neural tissue damage and the associated mechanisms in neuronal repair, highlighting the role of B cells along with VGLUT1/VGLUT2 (vesicular glutamate transporter 1/2) terminals and glutamate AMPA receptors, IL-1R1 signalling, and ERK/Stat6/MERTK Signalling. Furthermore, it focuses on the types of biomaterials, their characteristics, and mechanisms to overcome neuronal damage repair challenges using modern biomaterial-dependent neuronal tissue engineering techniques. Axonal regeneration can be enhanced by mixing many components (biomaterials, cells, and chemicals) to recover from neural nerve illnesses. Polymers, such as collagen, gelatin, chitosan, alginate, hyaluronan, silk fibroin, poly(L-lactic acid), poly(glycolic acid), polycaprolactone, polyphosphoester, and polyurethane, have been used to aid nerve cell growth. These polymers can be either natural or synthetic. Biomaterials that conduct electricity, such as polypyrrole, polythiophene, and polyaniline, can help neurites grow and make cells more active because they carry electrical impulses that help nerve signal travel. The primary goal of this review is to examine the current methods and uses of brain tissue engineering techniques, which include aspects of stem cell-based 3D in vitro and in vivo models, translational efforts, and challenges in clinical applications.