Evidence map›Paper›PMID 41981183›Full record

ArticleScientific reports2026

Lactate treatment improves brain biochemistry and cognitive function in transgenic Alzheimer's and wild-type mice.

Imen Belhaj, Ingrid Åmellem, Can H Tartanoglu, Hanne M Weidemann, Evan M Vallenari, Mingyi Yang, Farrukh A Chaudhry, Magnar Bjørås, Jon Storm-Mathisen, Linda Hildegard Bergersen

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Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
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0citing papers in PubMed
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1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors.

Imen Belhaj *Brain and Muscle Energy Group, Institute of Oral Biology, University of Oslo, Oslo, Norway. belha@online.no.
Ingrid Åmellem *Brain and Muscle Energy Group, Institute of Oral Biology, University of Oslo, Oslo, Norway. ingrid.amellem@ntnu.no.
Can H TartanogluDepartment of Neurosciences, Charité University Hospital, The German Center for Neurodegenerative Diseases (DZNE), Berlin, Germany.
Hanne M WeidemannBrain and Muscle Energy Group, Institute of Oral Biology, University of Oslo, Oslo, Norway.
Evan M VallenariBrain and Muscle Energy Group, Institute of Oral Biology, University of Oslo, Oslo, Norway.
Mingyi YangCentre for Embryology and Healthy Development (CRESCO), University of Oslo, Oslo, 0373, Norway.
Farrukh A ChaudhryDivision of Anatomy, Department of Molecular Medicine, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway.
Magnar BjøråsCentre for Embryology and Healthy Development (CRESCO), University of Oslo, Oslo, 0373, Norway.
Jon Storm-MathisenDivision of Anatomy, Department of Molecular Medicine, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway.
Linda Hildegard BergersenBrain and Muscle Energy Group, Institute of Oral Biology, University of Oslo, Oslo, Norway.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lactate, a well-known metabolite and signalling molecule, holds therapeutic potential for neurodegenerative diseases. Here, we investigated the effects of chronic lactate treatment on cognition and molecular biomarkers in the 5XFAD mouse model of Alzheimer’s disease (AD) and in wild-type (WT) controls using behavioural testing alongside proteomic and transcriptomic analyses. Mice received lactate or vehicle injections 4 days per week for 11 weeks, with behavioural testing before and after the treatment period. Lactate improved working memory in late-treated AD mice, without eliciting anxiety-like behaviour. At the molecular level, lactate reduced Il1b expression, and in a sex-dependent manner, normalised NEFL, and enhanced synaptic integrity proteins (OPCML, PPFIA2, STXBP3, SYT1, VGLUT2, VSNL1) in AD mice, while also augmenting mitochondrial regulators (ATP5G2, GRPEL1, SLC25A23) across genotypes. Notably, lactate upregulated low-abundance ionotropic glutamate receptor mRNAs (Grik3, Grin2c, Grid2ip) in female AD mice, indicating enhanced glutamatergic signalling. In WT mice, lactate increased expression of neurotrophic factors (Bdnf, Igf1, Vegfa), anti-inflammatory cytokines (Il4 and Il13), and the neuronal lactate transporter Mct2, suggesting promoted neuronal resilience. Together, these findings indicate that lactate treatment can mitigate cognitive decline and enhance molecular pathways of resilience in AD, warranting larger, age-stratified studies to validate its therapeutic potential and elucidate underlying mechanisms.

Indexed as

Alzheimer DiseaseBrainCognitionLactic AcidAnimalsDisease Models, AnimalFemaleMaleMiceMice, TransgenicProteomicsLactic Acid5XFADAlzheimer’s diseaseGlutamate receptorsGrowth factorsLactateNeuroinflammation

Identifiers

PMID41981183
PMCPMC13260460

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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.