Fungal polysaccharide ATEP tested in sleep-deprived mice and LPS-stimulated microglia
In this abstract, the fungal polysaccharide ATEP improved cognitive and antioxidant measures and reduced neuroinflammation in sleep-deprived mice, and in cell experiments it shifted microglia from M1 to M2 polarization; the authors attribute this to inhibited mTOR signaling. These are preclinical findings, not evidence of benefit in humans. [1]
Automatic summary · not editorially reviewed
The key findings
ATEP was isolated from the fungus Armillariella tabescens at 99.3% purity with an average molecular weight of 39.17 kDa, and network pharmacology predicted IL-6, TNF-α, IL-1β and mTOR as core targets. [1]
In sleep-deprived mice, ATEP improved cognitive function, raised SOD, CAT and GSH, lowered IL-6, IL-1β and TNF-α, reduced APP, BACE1 and p-Tau, and inhibited neuronal apoptosis in the hippocampus; in BV2 cells it shifted M1 to M2 polarization and changed glycolytic and mitochondrial measures. [1]
The authors attribute the effects to inhibition of mTOR pathway activation driving glycolytic reprogramming and M1-to-M2 polarization, and present ATEP as a candidate for developing neuroprotective agents, not as a validated product. [1]
The source at a glance
- Study type / format
- Preclinical study combining network pharmacology prediction with in vivo mouse and in vitro cell experiments (abstract)
- Population / context
- Sleep-deprived mice in a neurodegenerative disease model and LPS-stimulated BV2 microglial cells in the laboratory
- Summary based on
- Study abstract
- Original publication
- August 4, 2026
ATEP tested in sleep-deprived mice and microglial cells
The researchers isolated and characterized a polysaccharide from the medicinal fungus Armillariella tabescens, called ATEP, at 99.3% purity with an average molecular weight of 39.17 kDa. They combined computer-based network pharmacology prediction with experiments in two models: a sleep-deprived mouse model of neurodegenerative disease and LPS-stimulated BV2 microglial cells in the laboratory. Network pharmacology pointed to IL-6, TNF-α, IL-1β and mTOR as core targets.
Supporting source [1]
Cognitive, antioxidant and inflammatory measures in mice
In the sleep-deprived mice, ATEP was reported to improve cognitive function and raise antioxidant capacity, with higher SOD, CAT and GSH. It suppressed neuroinflammation, with lower IL-6, IL-1β and TNF-α, and lowered neurotoxic proteins APP, BACE1 and p-Tau. It also inhibited neuronal apoptosis in the hippocampus. In the cell experiments, ATEP dose-dependently inhibited LPS-induced M1 polarization and promoted M2 polarization, reduced lactate, increased ATP, lowered the glycolytic enzyme Pfkfb3 and the glutaminolysis enzyme GLS, and improved mitochondrial function.
Supporting source [1]
Proposed mTOR-linked mechanism and preclinical scope
The authors conclude that ATEP works by inhibiting activation of the mTOR signaling pathway, which they say drives mTOR-dependent reprogramming of glycolytic metabolism and the shift of microglia from M1 to M2 polarization, thereby strengthening antioxidant defenses, reducing neuroinflammation and preserving synaptic integrity. They describe ATEP as a structurally defined natural candidate for developing metabolism-targeting neuroprotective agents against neurodegenerative diseases. This is a proposed mechanism and a candidate for further development, not a validated or approved product.
Supporting source [1]
How to interpret this
This explainer is based only on the abstract; the full text was not reviewed. The work is preclinical, using a sleep-deprived mouse model and LPS-stimulated BV2 cells, so the findings do not establish benefits for human health or lifespan. The proposed mTOR-linked mechanism is the authors' interpretation, and ATEP is a research candidate, not a validated or approved product.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Zhang Y, Yang S, Ran S, Du M, Chen J, Cen M, Gu Y, Liao J, Liu Y, Zhang R, Wang J. · europepmc.org · August 4, 2026