ArticleBehavioural brain research2020
Effects of dietary 5-methoxyindole-2-carboxylic acid on brain functional recovery after ischemic stroke.
Article in Behavioural brain research, 2020. 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.
The trial behind it
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Renoprotection by 5-Methoxytryptophan in Kidney Disease.Biomolecules · 2026Review
- Decreased hippocampal neurogenesis and post-stroke depression.Frontiers in psychiatry · 2026Review
- Exploring genetic associations and drug targets for mitochondrial proteins and schizophrenia risk.Schizophrenia (Heidelberg, Germany) · 2025Article
- Discovery of a New Polymorph of 5-Methoxy-1Molecules (Basel, Switzerland) · 2024Article
- Impact of daily administration of blackberry extract on gerbil model of transient cerebral ischemia.Acta cirurgica brasileira · 2024Article
- Roles of Dihydrolipoamide Dehydrogenase in Health and Disease.Antioxidants & redox signaling · 2023Review
- 5-Methoxyindole-2-Carboylic Acid (MICA) Fails to Retard Development and Progression of Type II Diabetes in ZSF1 Diabetic Rats.Reactive oxygen species (Apex, N.C.) · 2020Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Stroke leads to devastating outcomes including impairments of sensorimotor and cognitive function that may be long lasting. New intervention strategies are needed to overcome the long-lasting effects of ischemic injury. Previous studies determined that treatment with 5-methoxyindole-2-carboxylic acid (MICA) conferred chemical preconditioning and neuroprotection against stroke. The purpose of the current study was to determine whether the preconditioning can lead to functional improvements after stroke (done by transient middle cerebral artery occlusion). After 4 weeks of MICA feeding, half the rats underwent ischemic injury, while the other half remained intact. After one week recovery, all the rats were tested for motor and cognitive function (rotorod and water maze). At the time of euthanasia, measurements of long-term potentiation (LTP) were performed. While stroke injury led to motor and cognitive dysfunction, MICA supplementation did not reverse these impairments. However, MICA supplementation did improve stroke-related impairments in hippocampal LTP. The dichotomy of the outcomes suggest that more studies are needed to determine optimum duration and dosage for MICA to lead to substantial motor and cognitive improvements, along with LTP change and neuroprotection.
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Registered trials
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 OpenQuestion graph.