Component
Human excitatory amino acid transporter 2 / SLC1A2
Human excitatory amino acid transporter 2 / SLC1A2
1 recorded relationships. Experimental role, claim status and evidence remain attached to each record.
How nutrients influence it
Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
How nutrients reach it in more than one step
Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.
Tracing routes…
What it does
Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.
What acts on it
Frontal-cortex EAAT2 protein was 71% lower in the five Wernicke cases than in five controls.
Experimental context and source evidence
- availability_state
- nutrient_deficiency Imported condition classification; unverified.
- evidence_location
- Abstract; Results; Figure 1
- evidence_span
- diminished by 71%
- experimental_model
- Human frontal-cortex autopsy samples: five male Wernicke encephalopathy cases with alcohol intake above 80 g/day versus five male controls below 20 g/day; immunoblotting and histology.
- exposure
- Neuropathologically identified Wernicke encephalopathy with heavy alcohol exposure
- limitations
- Does not isolate thiamine from alcohol effects, establish the initiating event, or directly measure uptake in living patients.
- nutrient_topic
- Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
- organism
- Homo sapiens
- plain_language
- An astrocyte glutamate transporter was reduced in the sampled diseased human cortex.
- primary_references
- [hazell-2010-human-astrocytes] Loss of astrocytic glutamate transporters in Wernicke encephalopathy (2010). https://pmc.ncbi.nlm.nih.gov/articles/PMC3388119/ DOI: 10.1002/glia.20908
- tissue_or_cell_type
- Frontal cortex
- trigger_kind
- nutrient_deficiency Imported condition classification; unverified.
Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1269–1281
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human frontal-cortex autopsy samples: five male Wernicke encephalopathy cases with alcohol intake above 80 g/day versus five male controls below 20 g/day; immunoblotting and histology. · source_derived_draft · unverified_draft
### thiamine-def-human-eaat2-loss Frontal-cortex EAAT2 protein was 71% lower in the five Wernicke cases than in five controls. Condition category: nutrient_deficiency nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: An astrocyte glutamate transporter was reduced in the sampled diseased human cortex. organism: Homo sapiens tissue_or_cell_type: Frontal cortex experimental_model: Human frontal-cortex autopsy samples: five male Wernicke encephalopathy cases with alcohol intake above 80 g/day versus five male controls below 20 g/day; immunoblotting and histology. limitations: Does not isolate thiamine from alcohol effects, establish the initiating event, or directly measure uptake in living patients. evidence_location: Abstract; Results; Figure 1 evidence_span: diminished by 71% exposure: Neuropathologically identified Wernicke encephalopathy with heavy alcohol exposure [hazell-2010-human-astrocytes] Loss of astrocytic glutamate transporters in Wernicke encephalopathy (2010). https://pmc.ncbi.nlm.nih.gov/articles/PMC3388119/ DOI: 10.1002/glia.20908
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.