Article in Stroke, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
2 · The registry
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what money
Authors and funding
26 authors.
Francisco J De Castro-Millán *Cardiovascular Risk Factors and Brain Health Programme, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain (F.J.D.C.-M., S.V.-R., C.P.-M., A.R.-L., C.P.-P., C.N.-V., A.G.-C., M.I.C., M.A.M.).ORCID 0009-0002-1004-0367
Sandra Vázquez-Reyes *Cardiovascular Risk Factors and Brain Health Programme, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain (F.J.D.C.-M., S.V.-R., C.P.-M., A.R.-L., C.P.-P., C.N.-V., A.G.-C., M.I.C., M.A.M.).ORCID 0000-0002-7365-975X
Carolina Peña-MartínezCardiovascular Risk Factors and Brain Health Programme, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain (F.J.D.C.-M., S.V.-R., C.P.-M., A.R.-L., C.P.-P., C.N.-V., A.G.-C., M.I.C., M.A.M.).ORCID 0000-0002-6904-8841
Adrián Rodríguez-LlaveCardiovascular Risk Factors and Brain Health Programme, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain (F.J.D.C.-M., S.V.-R., C.P.-M., A.R.-L., C.P.-P., C.N.-V., A.G.-C., M.I.C., M.A.M.).
Carlos Parra-PérezCardiovascular Risk Factors and Brain Health Programme, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain (F.J.D.C.-M., S.V.-R., C.P.-M., A.R.-L., C.P.-P., C.N.-V., A.G.-C., M.I.C., M.A.M.).ORCID 0009-0007-3817-1445
Carmen Nieto-VaqueroCardiovascular Risk Factors and Brain Health Programme, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain (F.J.D.C.-M., S.V.-R., C.P.-M., A.R.-L., C.P.-P., C.N.-V., A.G.-C., M.I.C., M.A.M.).ORCID 0009-0002-1653-9943
Gaia BrezzoUK Dementia Research Institute (G.B., D.S., B.W.M.), University of Edinburgh.ORCID 0000-0002-7523-8860
Kristy A ZeraDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, CA (K.A.Z., M.S.B.).ORCID 0000-0001-9178-6907
Dana StrausUK Dementia Research Institute (G.B., D.S., B.W.M.), University of Edinburgh.
Jennifer E GoertzThe Feil Family Brain and Mind Research Institute, Weill Cornell Medicine, New York, NY (J.E.G., J.A.).ORCID 0000-0003-4883-1586
Sanna H LoppiDepartment of Immunobiology, University of Arizona, Tucson (S.H.L., R.R.C., J.B.F., D.A.B., K.P.D.).ORCID 0000-0002-8848-0453
Rachel R CrumpackerDepartment of Immunobiology, University of Arizona, Tucson (S.H.L., R.R.C., J.B.F., D.A.B., K.P.D.).
Jennifer B FryeDepartment of Immunobiology, University of Arizona, Tucson (S.H.L., R.R.C., J.B.F., D.A.B., K.P.D.).
Danielle A BecktelDepartment of Immunobiology, University of Arizona, Tucson (S.H.L., R.R.C., J.B.F., D.A.B., K.P.D.).ORCID 0000-0002-8463-0282
Claudia DamesDepartment of Neurology with Experimental Neurology, Center for Stroke Research Berlin, Charité-Universitätsmedizin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Germany (C.D., D.B., A.M.).ORCID 0000-0002-9030-9532
Daniel BerchtoldDepartment of Neurology with Experimental Neurology, Center for Stroke Research Berlin, Charité-Universitätsmedizin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Germany (C.D., D.B., A.M.).ORCID 0000-0002-7865-4157
Jill H FowlerInstitute for Neuroscience and Cardiovascular Research (G.B., D.S., J.H.F., B.W.M.), University of Edinburgh.ORCID 0000-0003-3204-1221
Andreas MeiselDepartment of Neurology with Experimental Neurology, Center for Stroke Research Berlin, Charité-Universitätsmedizin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Germany (C.D., D.B., A.M.).ORCID 0000-0001-7233-5342
Josef AnratherThe Feil Family Brain and Mind Research Institute, Weill Cornell Medicine, New York, NY (J.E.G., J.A.).ORCID 0000-0002-0468-9162
Kristian P DoyleDepartment of Immunobiology, University of Arizona, Tucson (S.H.L., R.R.C., J.B.F., D.A.B., K.P.D.).ORCID 0000-0003-2788-7038
Stuart M AllanDivision of Neuroscience, School of Biological Sciences, Faculty of Biology, Medicine and Health, The University of Manchester, United Kingdom (S.M.A.).ORCID 0000-0001-9646-4456
Marion S BuckwalterDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, CA (K.A.Z., M.S.B.).ORCID 0000-0003-2807-2447
Barry W McCollUK Dementia Research Institute (G.B., D.S., B.W.M.), University of Edinburgh.ORCID 0000-0002-0521-9656
Alicia García-CulebrasCardiovascular Risk Factors and Brain Health Programme, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain (F.J.D.C.-M., S.V.-R., C.P.-M., A.R.-L., C.P.-P., C.N.-V., A.G.-C., M.I.C., M.A.M.).ORCID 0000-0003-2362-0117
María Isabel CuarteroCardiovascular Risk Factors and Brain Health Programme, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain (F.J.D.C.-M., S.V.-R., C.P.-M., A.R.-L., C.P.-P., C.N.-V., A.G.-C., M.I.C., M.A.M.).ORCID 0000-0003-4728-068X
María Ángeles MoroCardiovascular Risk Factors and Brain Health Programme, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain (F.J.D.C.-M., S.V.-R., C.P.-M., A.R.-L., C.P.-P., C.N.-V., A.G.-C., M.I.C., M.A.M.).ORCID 0000-0003-1010-8237
Funding
No grant is acknowledged in the PubMed record.
6 · The paper itself
Abstract
backgroundAdult hippocampal neurogenesis is altered after cerebral ischemia. Although stroke increases newborn neuron production, many cells display aberrant morphological and positional features that may impair functional integration and contribute to long-term cognitive deficits. Given the clinical heterogeneity of ischemic stroke and limited translational success of preclinical studies relying on single models, it remains unclear whether poststroke neurogenic alterations are conserved across experimental paradigms. This study aimed to identify common and model-specific features of hippocampal neurogenesis across focal ischemia models.
methodsWe conducted a multicenter, multimodel analysis within the Leducq-funded Stroke-Impact Transatlantic Network of Excellence using permanent and transient middle cerebral artery occlusion paradigms, including distal middle cerebral artery occlusion under normoxic or hypoxic conditions (distal middle cerebral artery occlusion+hypoxia), and filament-based transient middle cerebral artery occlusion, across 6 sites. Adult C57BL/6J mice were analyzed at 3 days, 7 days, and 2 months after ischemia, sham, or naïve conditions. Hippocampal proliferation (Ki67) and neuroblasts (DCX [doublecortin]) were quantified; morphological maturation of newborn neurons was assessed through high-resolution analyses of dendritic architecture and somatodendritic polarity.
resultsAcross all stroke models, ischemia induced a robust bilateral increase in hippocampal proliferation, most pronounced at 3 days and still elevated at 7 days, returning to baseline by 2 months. Neuroblast density was similarly increased at 7 days, particularly in the ipsilateral hippocampus, but normalized over time. Despite recovery in cell number, long-term analyses revealed a consistent reduction in apical dendrite length and increased proportion of neurons with aberrant features, including ectopic positioning, polarity defects, and abnormal lateral growth, across models and centers.
conclusionsAberrant hippocampal neurogenesis represents a robust hallmark of poststroke pathology in mice, independent of ischemia type or surgical approach, despite known differences in the spatial distribution of primary injury across models. Our findings underscore the importance of considering structural quality, and not only quantity, of newborn neurons when evaluating poststroke plasticity and developing therapeutic strategies.
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.
Aberrant Hippocampal Neurogenesis Is a Conserved Response to Stroke in Mice: A Multicenter Multimodel Study. · full record | Socratic