{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,5]],"date-time":"2026-11-05T04:29:48Z","timestamp":1793852988247,"version":"4.6.1"},"reference-count":183,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"4","license":[{"start":{"date-parts":[[2025,6,19]],"date-time":"2025-06-19T00:00:00Z","timestamp":1750291200000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-sa\/4.0"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2026,4]]},"abstract":"<jats:p>Neurodevelopmental and neurodegenerative illnesses constitute a global health issue and a foremost economic burden since they are a large cause of incapacity and death worldwide. Altogether, the burden of neurological disorders has increased considerably over the past 30 years because of population aging. Overall, neurological diseases significantly impair cognitive and motor functions and their incidence will increase as societies age and the world\u2019s population continues to grow. Autism spectrum disorder, motor neuron disease, encephalopathy, epilepsy, stroke, ataxia, Alzheimer\u2019s disease, amyotrophic lateral sclerosis, Huntington\u2019s disease, and Parkinson\u2019s disease represent a non-exhaustive list of neurological illnesses. These affections are due to perturbations in cellular homeostasis leading to the progressive injury and death of neurons in the nervous system. Among the common features of neurological handicaps, we find protein aggregation, oxidative stress, neuroinflammation, and mitochondrial impairment in the target tissues, e.g., the brain, cerebellum, and spinal cord. The high energy requirements of neurons and their inability to produce sufficient adenosine triphosphate by glycolysis, are responsible for their dependence on functional mitochondria for their integrity. Reactive oxygen species, produced along with the respiration process within mitochondria, can lead to oxidative stress, which compromises neuronal survival. Besides having an essential role in energy production and oxidative stress, mitochondria are indispensable for an array of cellular processes, such as amino acid metabolism, iron-sulfur cluster biosynthesis, calcium homeostasis, intrinsic programmed cell death (apoptosis), and intraorganellar signaling. Despite the progress made in the last decades in the understanding of a growing number of genetic and molecular causes of central nervous diseases, therapies that are effective to diminish or halt neuronal dysfunction\/death are rare. Given the genetic complexity responsible for neurological disorders, the development of neuroprotective strategies seeking to preserve mitochondrial homeostasis is a realistic challenge to lastingly diminish the harmful evolution of these pathologies and so to recover quality of life. A promising candidate is the neuroglobin, a globin superfamily member of 151 amino acids, which is found at high levels in the brain, the eye, and the cerebellum. The protein, which localizes to mitochondria, is involved in electron transfer, oxygen storage and defence against oxidative stress; hence, possessing neuroprotective properties. This review surveys up-to-date knowledge and emphasizes on existing investigations regarding neuroglobin physiological functions, which remain since its discovery in 2000 under intense debate and the possibility of using neuroglobin either by gene therapy or its direct delivery into the brain to treat neurological disorders.<\/jats:p>","DOI":"10.4103\/nrr.nrr-d-24-01503","type":"journal-article","created":{"date-parts":[[2025,6,19]],"date-time":"2025-06-19T15:02:15Z","timestamp":1750345335000},"page":"1292-1303","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":6,"title":["Neuroglobin: A promising candidate to treat neurological diseases"],"prefix":"10.4103","volume":"21","author":[{"given":"Ivan Millan","family":"Ya\u00f1ez","sequence":"first","affiliation":[{"name":"Department of Physiology, University of Valencia, Valencia, Spain"},{"name":"Neonatal Research Group, Health Research Institute La Fe (IISLAFE), Valencia, Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8098-1106","authenticated-orcid":false,"given":"Isabel","family":"Torres-Cuevas","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of Valencia, Valencia, Spain"},{"name":"Neonatal Research Group, Health Research Institute La Fe (IISLAFE), Valencia, Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2854-9997","authenticated-orcid":false,"given":"Marisol","family":"Corral-Debrinski","sequence":"additional","affiliation":[{"name":"Universit\u00e9 Paris Cit\u00e9, NeuroDiderot, Inserm, Paris, France"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","published-online":{"date-parts":[[2025,6,19]]},"reference":[{"key":"R1-20260421","doi-asserted-by":"crossref","first-page":"188","DOI":"10.3389\/fncel.2018.00188","article-title":"Novel Nrf2-inducer prevents mitochondrial defects and oxidative stress in Friedreich\u2019s ataxia models","volume":"12","author":"Abeti","year":"2018","journal-title":"Front Cell Neurosci"},{"key":"R2-20260421","doi-asserted-by":"crossref","first-page":"2756","DOI":"10.1111\/ejn.14731","article-title":"Insight into the molecular sex dimorphism of ischaemic stroke in rat cerebral cortex: Focus on neuroglobin, sex steroids and autophagy","volume":"52","author":"Acaz-Fonseca","year":"2020","journal-title":"Eur J Neurosci"},{"key":"R3-20260421","doi-asserted-by":"crossref","first-page":"1502","DOI":"10.1038\/cdd.2016.36","article-title":"Metabolic reprogramming during neuronal differentiation","volume":"23","author":"Agostini","year":"2016","journal-title":"Cell Death Differ"},{"key":"R4-20260421","doi-asserted-by":"crossref","first-page":"e14217","DOI":"10.1111\/eci.14217","article-title":"Primary mitochondrial diseases: The intertwined pathophysiology of bioenergetic dysregulation, oxidative stress and neuroinflammation","volume":"54","author":"Aguilar","year":"2024","journal-title":"Eur J Clin Invest"},{"key":"R5-20260421","doi-asserted-by":"crossref","first-page":"893","DOI":"10.3390\/membranes12090893","article-title":"Mitochondrial fission and fusion: Molecular mechanisms, biological functions, and related disorders","volume":"12","author":"Al Ojaimi","year":"2022","journal-title":"Membranes (Basel)"},{"key":"R6-20260421","doi-asserted-by":"crossref","first-page":"83","DOI":"10.1016\/j.mito.2023.05.007","article-title":"Mitochondrial dysfunction and oxidative stress in Alzheimer\u2019s disease, and Parkinson\u2019s disease, Huntington\u2019s disease and amyotrophic lateral sclerosis-An updated review","volume":"71","author":"Alqahtani","year":"2023","journal-title":"Mitochondrion"},{"key":"R7-20260421","doi-asserted-by":"crossref","first-page":"151","DOI":"10.1111\/jnc.13876","article-title":"Neuroglobin protects astroglial cells from hydrogen peroxide-induced oxidative stress and apoptotic cell death","volume":"140","author":"Amri","year":"2017","journal-title":"J Neurochem"},{"key":"R8-20260421","doi-asserted-by":"crossref","first-page":"1","DOI":"10.1016\/j.mam.2016.10.004","article-title":"Neuroglobin: From structure to function in health and disease","volume":"52","author":"Ascenzi","year":"2016","journal-title":"Mol Aspects Med"},{"key":"R9-20260421","doi-asserted-by":"crossref","first-page":"1769","DOI":"10.1113\/EP088005","article-title":"Oxygen and brain death; 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