{"doi":"10.1002/nep3.57","title":"Effects of immunological processes and mild ambient atmosphere alterations on the brain in health and disease","abstract":"Immunological processes in the brain and periphery are well known to affect brain function in health and disease. However, our knowledge about the crosstalk between the immune system and the central nervous system is far from being complete. Ongoing research in this field is uncovering the complex interactions between these “supersystems,” often involving additional organs such as the gut with its microbiome, as well as pathophysiological factors such as hyperglycemia, hypertension, or dyslipidemia.1-3 Augmenting our knowledge of these complex interactions has the potential to increase diagnostic and prognostic precision and could lead to the discovery of novel therapeutic targets. Alterations of the ambient atmosphere have been investigated as potential approaches to improve brain function, primarily under pathological conditions. Prominent examples include hyperbaric oxygenation and the application of noble gases in acute ischemic stroke.4, 5 Although these approaches have not yet been translated into clinical routine applications, the underlying concepts have remained influential, informing alternative approaches that have been explored subsequently. One of the most intriguing concepts is to provide cerebroprotection by preconditioning, which can be achieved by applying hyperoxygenation as well as hypooxygenation.6, 7 Since these concepts can be applied easily and widely, they may help to augment our therapeutic arsenal against numerous conditions. However, the mechanisms involved, as well as certain safety concerns, require further detailed investigation. This issue of Neuroprotection features original contributions, including clinical investigations, and reviews that offer new insights into the impact of neuroimmunological processes and mild ambient atmosphere alterations on the brain in health and disease. These studies report promising approaches to improve diagnosis, potential therapeutic targets or concepts to improve brain performance under normal conditions. Key findings presented by these articles will be summarized in this editorial, also briefly discussing the potential future impact of the reported findings. Olajide et al. provide a comprehensive review on microglial senescence in the context of neurodegeneration. Senescent microglia are characterized by prolonged inflammatory responses and reduced dendritic branching, indicating a reduced capacity to polarize into a proregenerative, anti-inflammatory state which can support functional recuperation.8 The review offers detailed insights into alterations of microglial reactivity in neurodegenerative conditions, including changes occurring in senescent microglia such as iron overload and telomere shortening. Interestingly, senescent microglia encompass various states of activation. While they are predominantly proinflammatory the existence of these senescent cells challenges the classical M1/M2 discrimination between pro- and anti-inflammatory microglia. Based on a description of potential senescent microglia markers, the review then summarizes what is known about their role in different neurodegenerative diseases. This is important since identifying senescent microglia is an essential step in dicovering potential new therapeutic targets, and eventually improving the prospects of patients suffering from incurable conditions such as Alzheimer's disease.9 Results from a clinical study are reported by Tang et al. who retrospectively investigated the impact of the neutrophil-to-lymphocyte (NLR) ratio and hyperglycemia on clinical outcome of stroke patients undergoing recanalization by endovascular thrombectomy. Hyperglycemia at admission was negatively associated with a good functional outcome as defined by functional independence in patients with a low NLR ratio, but not in those exhibiting a high NLR ratio. However, the interaction between NLR ratio and hyperglycemia did not predict hemorrhagic transformation or mortality 3 months after stroke. This suggests that pat","journal":"Neuroprotection/Neuroprotection (Chichester, England. Print)","year":2024,"id":503154,"datarank":0.0,"base_score":0.0,"endowment":0.0,"self_citation_contribution":0.0,"citation_network_contribution":0.0,"self_endowment_contribution":0.0,"citer_contribution":0.0,"corpus_percentile":null,"corpus_rank":null,"citation_count":0,"citer_count":0,"citers_with_citation_signal":0,"citers_with_endowment":0,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":0.9504,"is_data_producer":false,"deposit_databanks":null,"is_oa":true,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":"2024-01-01","fair_score":null,"fair_percentile":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":320471,"name":"Xunming Ji","orcid":"0000-0003-0293-2744","position":1,"is_corresponding":false},{"id":746253,"name":"Shen Li","orcid":"0000-0001-6779-9812","position":2,"is_corresponding":false},{"id":851068,"name":"Johannes Boltze","orcid":"0000-0003-3956-4164","position":3,"is_corresponding":false},{"id":416236,"name":"Piotr Walczak","orcid":"0000-0002-3733-3322","position":0,"is_corresponding":true}],"reference_count":11,"raw_metadata":null,"created_at":"2026-07-19T02:10:27.781502Z","pmid":"39346949","pmcid":null,"fwci":null,"citation_percentile":null,"influential_citations":0,"oa_status":null,"license":null,"views":0,"total_file_size_bytes":0,"version_count":0,"fair_f":null,"fair_a":null,"fair_i":null,"fair_r":null,"fair_zscore":null,"fair_rationale":null,"fair_model":null,"fair_agent_version":null,"fair_fulltext_source":null,"fair_has_llm":null,"fair_computed_at":null,"clinical_trials":[],"software_tools":[],"db_accessions":[],"linked_datasets":[],"topics":[]}