Component
Experimental RBM3 knockdown in mouse hippocampus
Experimental RBM3 knockdown in mouse hippocampus. Species, exposure and limitations are retained in each linked claim.
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.
Where it participates (unsigned role)
Enhanced RBM3 expression, achieved either by hypothermia before the loss of the response or by lentiviral delivery, restored synapse reassembly, gave sustained synaptic protection, prevented behavioural deficits and neuronal loss and significantly prolonged survival, whereas RBM3 knockdown exacerbated synapse loss, accelerated disease and prevented the neuroprotective effects of cooling.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/cold-research/25607368.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d5cf22cc43a38b28c13d58f29dc4ada326eb6617d86ea4a704638c675406cf48", "start_char": 0, "end_char": 2081, "text_sha256": "d5cf22cc43a38b28c13d58f29dc4ada326eb6617d86ea4a704638c675406cf48"}
- experimental_model
- Cooled laboratory rodents and mouse models of prion disease and Alzheimer-type neurodegeneration
- exposure
- Artificial cooling with rewarming; RBM3 overexpression or knockdown
- limitations
- A strong causal design in disease models, using both overexpression and knockdown. It is cooling of anaesthetised rodents, not cold water immersion of a person.
- nutrient_topic
- Cold water immersion research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Cold water immersion
- organism
- Mouse
- plain_language
- Raising the cold protein protected the brain and extended life; removing it cancelled the benefit of cooling itself.
- primary_references
- [cold-p25607368] RBM3 mediates structural plasticity and protective effects of cooling in neurodegeneration. (2015). https://pubmed.ncbi.nlm.nih.gov/25607368/ DOI: 10.1038/nature14142
- tissue_or_cell_type
- Hippocampus and synapses
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Cold water immersion: cold sensing, heat production, the catecholamine axis and what repeated exposure changes (2026-09-19) · lines 923–934
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cooled laboratory rodents and mouse models of prion disease and Alzheimer-type neurodegeneration · source_derived_draft · unverified_draft
### cold-rbm3-neuroprotection Enhanced RBM3 expression, achieved either by hypothermia before the loss of the response or by lentiviral delivery, restored synapse reassembly, gave sustained synaptic protection, prevented behavioural deficits and neuronal loss and significantly prolonged survival, whereas RBM3 knockdown exacerbated synapse loss, accelerated disease and prevented the neuroprotective effects of cooling. Condition category: machinery_impairment nutrient_topic: Cold water immersion research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: Raising the cold protein protected the brain and extended life; removing it cancelled the benefit of cooling itself. organism: Mouse tissue_or_cell_type: Hippocampus and synapses experimental_model: Cooled laboratory rodents and mouse models of prion disease and Alzheimer-type neurodegeneration limitations: A strong causal design in disease models, using both overexpression and knockdown. It is cooling of anaesthetised rodents, not cold water immersion of a person. exposure: Artificial cooling with rewarming; RBM3 overexpression or knockdown evidence_span: {"source_cache": "artifacts/cold-research/25607368.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d5cf22cc43a38b28c13d58f29dc4ada326eb6617d86ea4a704638c675406cf48", "start_char": 0, "end_char": 2081, "text_sha256": "d5cf22cc43a38b28c13d58f29dc4ada326eb6617d86ea4a704638c675406cf48"} [cold-p25607368] RBM3 mediates structural plasticity and protective effects of cooling in neurodegeneration. (2015). https://pubmed.ncbi.nlm.nih.gov/25607368/ DOI: 10.1038/nature14142
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.