Lactate restores PGC1α and BDNF expression rescuing cognitive impairments in a mouse model for schizophrenia.
Level 5 - mechanism / opinion, no new human data
Animal research (preclinical mouse model)
PubMed 41707874 · doi:10.1016/j.bbr.2026.116111
What was done
Adult male and female wildtype mice and 4cG transgenic mice (a psychosis model with 4 copies of the Gldc gene) received acute intraperitoneal L-lactate one hour before testing. The researchers evaluated behaviors using the Y-maze spontaneous alternation test, prepulse inhibition of acoustic startle, and the three-chamber social interaction test, followed by Western blots on brain tissue for PGC1α and BDNF protein levels.
What was found
The abstract reports no numerical values or effect sizes. Acute lactate administration in 4cG mice reportedly rescued short-term memory deficits, acoustic startle habituation deficits, and social preference deficits, while restoring PGC1α and BDNF protein expression.
Why it matters
This study provides preclinical evidence that targeting astrocytic metabolic support via exogenous lactate can acutely reverse specific cognitive, behavioral, and molecular deficits in a genetic mouse model of schizophrenia.
Limits
The study is in a rodent model and cannot establish efficacy or safety in humans. The abstract does not report sample sizes, specific quantitative data, dose-response relationships, or the long-term durability of the effects beyond acute one-hour administration.
Cited by
- supports Astrocytes are highly glycolytic and produce lactate from glucose, which is shuttled into neurons as an energy source and acts as a signaling molecule that affects BDNF.