{"doi":"10.1002/nep3.31","title":"Exploring novel experimental treatments for major neurodegenerative disorders","abstract":"Acute and chronic neurodegenerative disorders such as ischemic stroke or Alzheimer's disease (AD) impose a major burden on patients, their relatives, caregivers, and health care systems in general. The socioeconomic impact of neurodegenerative disorders is anticipated to escalate due to a globally ageing population and the increasing prevalence of sedentary lifestyle and inappropriate dietary habits. On the contrary, there is a paucity of therapeutic options providing causative treatment for neurodegenerative disorders, effectively mitigating their consequences and enhancing patients' quality of life. The few therapeutic options being available are often limited by temporal restrictions. For instance, recanalization approaches for ischemic stroke have a narrow therapeutic time window, rendering them inaccesible for the majority of patients. Current work therefore focuses on improving acute stroke management including adjuvant neuroprotective or immunomodulative interventions to allow more patients to benefit from recanalization.1 Similarly, recent approaches to target amyloid β (Aβ) plaques using monoclonal antibodies in AD are only effective in the early stages of the disease. However, the overall therapeutic impact remains modest, accompanied by the potential of severe side effects.2 Hence, there is a pressing need for novel therapeutic approaches. This issue of Neuroprotection features some exciting updates on experimental therapeutic research for neurodegenerative diseases, complemented by meta-analyses and reviews of previous, current, and future approaches. This editorial will summarize and highlight the most important aspects presented within these contributions. Liu et al. suggest an orchestrated, global strategy to combat AD, through the AD Neuroprotection Research Initiative (ADNRI). In their comprehensive assessment of current therapeutic opportunities for AD, they stress the importance of neuroimaging approaches at both cellular and system levels for clinical disease monitoring and translational activities. They also discuss current as well as potential future approaches for neuroprotective interventions in AD, providing a detailed overview of neurotrophic factors and anti-inflammatory treatments. They further highlight the role of astrocytes and oligodendrocytes in AD. They finally focus on metabolic, vascular, and meningeal aspects of AD, as well as potential peripheral interventions and lifestyle changes, thus offering a holistic picture of therapeutic opportunities. The work by Taguchi et al. interconnects with the insights offered by Liu and colleagues. The modest impact of anti-Aβ immunotherapies3 indirectly suggests that Aβ may not singularily constitute the entire pathomechanism in AD and consequently, may not be the only therapeutic target. The authors advocate for exploring potential targets such as the hippocampal neurogenesis as a viable avenue. Their rationale is based on the noteable decline in hippocampal neurogenesis among AD patients.4 Taguchi et al. not only provide a detailed rationale for their suggestion but also highlight the need for combination treatments to counter the complex AD pathology. They also claim that cell-based interventions hold promise for improving hippocampal neurogenesis. Cell-based interventions for hypoxic–ischemic encephalopathy (HIE) in newborns are investigated by Scrutton and colleagues. Performing a systematic literature review and meta-analysis, they compared the therapeutic impact of mononuclear cells (MNCs) in preclinical versus clinical studies in HIE. MNCs are a stem cell-containing population that can be obtained from umbilical cord blood or bone marrow and that is commonly used in early-stage clinical investigations due to their excellent safety profile and the use for swift, autologous application. There were no strong indicators for MNC efficacy in the early clinical studies included in the analysis, but clear indications for major design differences between ","journal":"Neuroprotection/Neuroprotection (Chichester, England. Print)","year":2023,"id":401958,"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":1,"citer_count":0,"citers_with_citation_signal":0,"citers_with_endowment":0,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":0.9581,"is_data_producer":false,"deposit_databanks":null,"is_oa":true,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":"2023-01-01","fair_score":null,"fair_percentile":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":416236,"name":"Piotr Walczak","orcid":"0000-0002-3733-3322","position":1,"is_corresponding":false},{"id":851068,"name":"Johannes Boltze","orcid":"0000-0003-3956-4164","position":2,"is_corresponding":false},{"id":1048539,"name":"Xunming Ji","orcid":"0000-0002-0527-2852","position":0,"is_corresponding":true}],"reference_count":5,"raw_metadata":null,"created_at":"2026-07-19T01:20:23.920156Z","pmid":"38179225","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":[]}