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Abolition of aberrant neurogenesis ameliorates cognitive impairment after stroke in mice
Open accessAbstract
Poststroke cognitive impairment is considered one of the main complications during the chronic phase of ischemic stroke. In the adult brain, the hippocampus regulates both encoding and retrieval of new information through adult neurogenesis. Nevertheless, the lack of predictive models and studies based on the forgetting processes hinders the understanding of memory alterations after stroke. Our aim was to explore whether poststroke neurogenesis participates in the development of long-term memory impairment. Here, we show a hippocampal neurogenesis burst that persisted 1 month after stroke and that correlated with an impaired contextual and spatial memory performance. Furthermore, we demonstrate that the enhancement of hippocampal neurogenesis after stroke by physical activity or memantine treatment weakened existing memories. More importantly, stroke-induced newborn neurons promoted an aberrant hippocampal circuitry remodeling with differential features at ipsi- and contralesional levels. Strikingly, inhibition of stroke-induced hippocampal neurogenesis by temozolomide treatment or using a genetic approach (Nestin-CreERT2/NSE-DTA mice) impeded the forgetting of old memories. These results suggest that hippocampal neurogenesis modulation could be considered as a potential approach for treatment of poststroke cognitive impairment.
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“Brain injury models, such as stroke, seizure, and blunt trauma, all increase the rate of adult neurogenesis (Table 1), yet each of these conditions is associated with reduced cognitive function (Cuartero et al., 2019; Parent and Lowenstein, 2002; Sun et al., 2015).”
From Adult neurogenesis, glia, and the extracellular matrix (2019) · cites this paper as Cuartero et al., 2019
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“In fact, inhibiting adult neurogenesis reduces the frequency of chronic seizures along with seizure-related cognitive decline (Cho et al., 2015) as well as stroke-induced cognitive decline (Cuartero et al., 2019).”
From Adult neurogenesis, glia, and the extracellular matrix (2019) · cites this paper as Cuartero et al., 2019
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Metadata
- Authors
- Cuartero, M. I., de la Parra, J., Pérez-Ruiz, A., Bravo-Ferrer, I., Durán-Laforet, V., García-Culebras, A., García-Segura, J. M., Dhaliwal, J., Frankland, P. W., Lizasoain, I., & Moro, M. Á.
- Affiliations
- Universidad Complutense de Madrid (ES)
- Hospital for Sick Children (CA)
- ORCID
- Venue
- Journal of Clinical Investigation
- Published
- 2019-02-25
- Volume
- 129
- Issue
- 4
- Pages
- 1536-1550
- ISSN
- 0021-9738 (ISSN-L)
- 1558-8238
- PMC
- PMC6436875
- OpenAlex
- W2913288555
- Cited by
- 128
- References
- 69
- Citations by year
- 2026: 15 · 2025: 17 · 2024: 8 · 2023: 23 · 2022: 18 · 2021: 18 · 2020: 18 · 2019: 11
- FWCI
- 6.12
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- DIGITAL.CSIC (Spanish National Research Council (CSIC)) (submittedVersion)
- Funders
- Ministerio de Economía y Competitividad (SAF2015-68632-R)
- Canadian Institutes of Health Research (143227_1)
- Instituto de Salud Carlos III (PI17/01601)
- Topics
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- post-stroke cognitive impairment, ischemic stroke, forgetting, contextual memory, spatial memory, physical activity, memantine, temozolomide, newborn neurons, therapeutic target
- MeSH terms
- Temozolomide, Animals, Hippocampus, Male, Mice, Transgenic, Stroke, Mice, Neurogenesis, Cognitive Dysfunction, Spatial Memory
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