Intermittent fasting and cognitive decline in D-galactose-induced aging rats
In male rats made to age with D-galactose, six weeks of intermittent fasting alongside that treatment was linked to better memory and learning, higher serum BHB and PI3K/AKT/GSK-3β involvement; a PI3K inhibitor weakened these effects. [1]
Automatic summary · not editorially reviewed
The key findings
Forty-six two-month-old male Sprague-Dawley rats were assigned to five groups, including D-galactose-induced aging with and without six weeks of intermittent fasting. [1]
Intermittent fasting improved recognition memory and spatial learning and memory, and a PI3K inhibitor (LY294002) attenuated these improvements. [1]
The authors say causal roles of ketone metabolism require further validation. [1]
The source at a glance
- Study type / format
- Animal study (abstract)
- Population / context
- 46 male Sprague-Dawley rats, two months old, with D-galactose-induced aging.
- Summary based on
- Study abstract
- Original publication
- May 28, 2026
D-galactose aging rats and intermittent fasting
The abstract describes a study in 46 male Sprague-Dawley rats, two months old, split into five groups: Control, D-galactose-induced aging, D-galactose plus intermittent fasting, D-galactose plus intermittent fasting plus LY294002 (a PI3K inhibitor), and D-galactose plus intermittent fasting plus solvent. Intermittent fasting was given for six weeks together with D-galactose treatment. The stated aim was to test whether fasting attenuates cognitive decline in these rats, at least partly in association with BHB elevation and modulation of PI3K/AKT/GSK-3β signaling.
Supporting source [1]
Memory, hippocampal neurons and BHB in fasting rats
Recognition memory and spatial learning and memory were tested with the novel object recognition and Morris water maze tests; the open field test assessed locomotor activity and anxiety-like behavior. According to the abstract, intermittent fasting improved recognition memory and spatial learning and memory, preserved hippocampal neuronal morphology, increased the proportion of morphologically normal CA1 neurons, raised serum BHB, reduced neuroinflammation and tau phosphorylation, and restored BDNF expression. Adding LY294002 weakened these improvements, which the authors take as support for involvement of the PI3K/AKT/GSK-3β pathway.
Supporting source [1]
Transcriptomic changes and limits of the rat findings
Transcriptomic analysis reportedly showed suppression of senescence-related genes and modulation of neuroprotective pathways. The authors conclude that fasting attenuated cognitive decline in these D-galactose-induced aging rats in association with higher BHB and modulation of the PI3K/AKT/GSK-3β pathway. They describe fasting as a possibly promising non-pharmacological option for age-related cognitive dysfunction, but state that causal roles of ketone metabolism need further validation. This is an abstract of an animal study; the full text was not reviewed, and the results do not establish benefits for human lifespan or cognition.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. This is a rat study using D-galactose-induced aging, so the findings do not establish human cognitive or lifespan benefits, and the authors note that causal roles of ketone metabolism need further validation.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Lin X, Huang L, Ling X, Lu J, Lin L, Ding L, Lin X, Chen T. · europepmc.org · May 28, 2026