ArticleNeurobiology of disease2016
Cognitive and behavior deficits in sickle cell mice are associated with profound neuropathologic changes in hippocampus and cerebellum.
Article in Neurobiology of disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 42 citations in OpenAlex.
- Simplified Procedure for Isolation and Culture of Neuronal Cells from Brains of Sickle Cell Mice.Cells · 2026Article
- NLRP3 inflammasome-mediated platelet hyperreactivity in sickle cell mice is targetable by BTK inhibition.Biochemical and biophysical research communications · 2026Article
- Pyruvate kinase deficiency modifies sickle hemoglobin carrier and sickle cell disease phenotypes in mice.JCI insight · 2026Article
- The small-molecule Syk inhibitor R788 inhibits hematopoiesis and worsens anemia in sickle cell disease mice.Blood vessels, thrombosis & hemostasis · 2026Article
- Predecompression and postdecompression cognitive and affective changes in Chiari malformation type I.Journal of neurosurgery · 2025Article
- Behavioral and transcriptional effects of age in HbSS-BERK humanized SCD mice.Journal of sickle cell disease · 2025Article
- Kininogen enhances seizure susceptibility in mice possibly through bradykinin-induced modulation of calcium transients in glutamatergic and GABAergic neurons.Frontiers in pharmacology · 2025Article
- ΔThe Journal of pharmacology and experimental therapeutics · 2024Article
- Calcium flux alterations in erythrocytes from sickle cell mice: The relevance of mean corpuscular volume.Blood cells, molecules & diseases · 2024Article
- Mouse models of sickle cell disease: Imperfect and yet very informative.Blood cells, molecules & diseases · 2024Review
- Nitrite decreases sickle hemoglobin polymerization in vitro independently of methemoglobin formation.Toxicology and applied pharmacology · 2023Article
- Molecular and environmental contributors to neurological complications in sickle cell disease.Experimental biology and medicine (Maywood, N.J.) · 2023Review
- White-matter abnormalities and cognitive dysfunction are linked to astrocyte activation in sickle mice.PNAS nexus · 2023Article
- Mitapivat increases ATP and decreases oxidative stress and erythrocyte mitochondria retention in a SCD mouse model.Blood cells, molecules & diseases · 2022Article
- Sickle cell disease as an accelerated aging syndrome.Experimental biology and medicine (Maywood, N.J.) · 2022Review
- MRI detection of brain abnormality in sickle cell disease.Expert review of hematology · 2021Article
- Sickle cell disease mice have cerebral oxidative stress and vascular and white matter abnormalities.Blood cells, molecules & diseases · 2021Article
- Analysis of hippocampal subfields in sickle cell disease using ultrahigh field MRI.NeuroImage. Clinical · 2021Article
- Role of age and neuroinflammation in the mechanism of cognitive deficits in sickle cell disease.Experimental biology and medicine (Maywood, N.J.) · 2021Article
- Elamipretide (SS-31) Improves Functional Connectivity in Hippocampus and Other Related Regions Following Prolonged Neuroinflammation Induced by Lipopolysaccharide in Aged Rats.Frontiers in aging neuroscience · 2021Article
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
Strokes are perhaps the most serious complications of sickle cell disease (SCD) and by the fifth decade occur in approximately 25% of patients. While most patients do not develop strokes, mounting evidence indicates that even without brain abnormalities on imaging studies, SCD patients can present profound neurocognitive dysfunction. We sought to evaluate the neurocognitive behavior profile of humanized SCD mice (Townes, BERK) and to identify hematologic and neuropathologic abnormalities associated with the behavioral alterations observed in these mice. Heterozygous and homozygous Townes mice displayed severe cognitive deficits shown by significant delays in spatial learning compared to controls. Homozygous Townes also had increased depression- and anxiety-like behaviors as well as reduced performance on voluntary wheel running compared to controls. Behavior deficits observed in Townes were also seen in BERKs. Interestingly, most deficits in homozygotes were observed in older mice and were associated with worsening anemia. Further, neuropathologic abnormalities including the presence of large bands of dark/pyknotic (shrunken) neurons in CA1 and CA3 fields of hippocampus and evidence of neuronal dropout in cerebellum were present in homozygotes but not control Townes. These observations suggest that cognitive and behavioral deficits in SCD mice mirror those described in SCD patients and that aging, anemia, and profound neuropathologic changes in hippocampus and cerebellum are possible biologic correlates of those deficits. These findings support using SCD mice for studies of cognitive deficits in SCD and point to vulnerable brain areas with susceptibility to neuronal injury in SCD and to mechanisms that potentially underlie those deficits.
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