Can Honey Protect Your Brain?โข Study Reviews Its Potential Against Alzheimer’s
A recent โreview โof laboratory studies suggests honey may offer โa surprising defense against alzheimer’s โฃDisease โข(AD).Published in Nutrients in 2025, the research, led by M.D. Navarro-Hortal and colleagues,โ examined a rangeโค of experiments – fromโข those โฃusing isolated cells to studies involving invertebrates like the โคnematodeโ Caenorhabditis elegans and the โฃfruit โfly Drosophila melanogaster, as โคwell as rodent models – to understand โคhow different โtypes โof honey impact AD pathology. The reviewโข considered the diverse sources and types of honey, โขincluding Manuka, Tualang,โ Chestnut, and Avocado varieties.
The findings indicateโ honey combats severalโข key hallmarks of AD, including oxidative stress,โข inflammation, โคand โคneurotransmitter imbalances. Researchers found honey and its extractsโค significantly reduced levelsโฃ of โฃreactive oxygen species (ROS),โค damaging molecules linked to cellular harm,โค in various models.
For example, chestnut-derived honey demonstrated antioxidative activity by protecting neuronal โcells from glutamate-induced damage and preserving mitochondrial function at concentrations between 500 and 750 โฃฮผg/mL. In C. elegans engineered to produce human amyloid-beta, both Manuka and avocado honeyโค (at 100 mg/mL) notably delayed the onset of โparalysis โคcaused by Aฮฒ. This suggestsโ a โฃpotent โขanti-inflammatory and anti-Aฮฒ efficacy. Interestingly, the study also revealed a paradoxical effect: in some worm models of tauopathy, honey โข worsened mobility, perhaps due โฃto its sugar content rather than a direct impact on tau.
These findings were further supported by experiments using murine models. Tualang honey reversed shiftsโ in hippocampal Aฮฒ1-40 and โขAฮฒ1-42 levels โขinduced by LPS, while โKelulut honey reduced โฃAฮฒ1-42 deposition โspecifically in the dentate gyrus, but not inโ the CA1 or CA3 regions of theโ brain. Furthermore, certainโข honeys exhibited the ability to inhibit โacetylcholinesterase, theโข enzyme โresponsible for breaking down acetylcholine – a โneurotransmitter crucial for memory. Acetylcholinesterase inhibitors areโค currently used as symptomatic treatments โfor AD.However, the review authors caution that results โคvaried significantly depending on the honey type, botanical source, processing methods, and study design. They also notedโข that many of the included studies โcarried a high or unclear risk of โคbias.
The review concludes that, in laboratoryโ and non-human models, honey demonstrates meaningful neuroprotective โคpotential, triggering benefits against the molecular drivers of AD by โreducing oxidative stress and inflammation and interfering withโ toxic protein โaggregation. Despite theseโฃ promising results, โthe authors emphasize a “stark lackโค of human-derivedโ evidence” and call for clinical trials to determine optimal dosages and establish quality guidelines for honey’s potential use in AD treatment.
Source: Navarro-Hortal, M. D., Romero-Mรกrquez, J. M.,Ansary,J.,โ Hinojosa-Nogueira, D., Montalbรกn-Hernรกndez, C., varela-Lรณpez, A., & Quiles, J.โฃ L. (2025). Honeyโฃ as a Neuroprotective Agent: molecular Perspectives on โขIts Role in Alzheimer’s disease. Nutrients,โข 17(16), 2577. DOI – 10.3390/nu17162577. https://www.mdpi.com/2072-6643/17/16/2577