ArticleMetabolic brain disease2016
Chronic methamphetamine exposure prior to middle cerebral artery occlusion increases infarct volume and worsens cognitive injury in Male mice.
Article in Metabolic brain disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Prelimbic cortex to zona incerta pathway mediates recognition memory recovery delay through down-regulating astrocytic GAT-3.iScience · 2026Article
- Maternal use of methamphetamine alters cardiovascular function in the adult offspring.Biochemistry and cell biology = Biochimie et biologie cellulaire · 2023Review
- Infusion of etoposide in the CA1 disrupts hippocampal immediate early gene expression and hippocampus-dependent learning.Scientific reports · 2022Article
- Methamphetamine-induced changes in myocardial gene transcription are sex-dependent.BMC genomics · 2021Article
- Short term methylphenidate treatment does not increase myocardial injury in the ischemic rat heart.Physiological research · 2020Article
- Impact of Methamphetamine Abuse: A Rare Case of Rapid Cerebral Aneurysm Growth with Review of Literature.Case reports in neurological medicine · 2018Article
- Repeated exposure to methamphetamine induces sex-dependent hypersensitivity to ischemic injury in the adult rat heart.PloS one · 2017Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Emerging evidence indicates that methamphetamine (MA) abuse can impact cardiovascular disease. In humans, MA abuse is associated with an increased risk of stroke as well as an earlier age at which the stroke occurs. However, little is known about how chronic daily MA exposure can impact ischemic outcome in either humans or animal models. In the present study, mice were injected with MA (10 mg/kg, i.p.) or saline once daily for 10 consecutive days. Twenty-four hours after the final injection, mice were subjected to transient middle cerebral artery occlusion (tMCAO) for one hour followed by reperfusion. Mice were tested for novel object memory at 96 h post-reperfusion, just prior to removal of brains for quantification of infarct volume using 2,3,5-Triphenyltetrazolium Chloride (TTC) staining. Mice treated with MA prior to tMCAO showed decreased object memory recognition and increased infarct volume compared to saline-treated mice. These findings indicate that chronic MA exposure can worsen both cognitive and morphological outcomes following cerebral ischemia.
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Registered trials
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