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Honey’s Neuroprotective Potential: Lab Study on Alzheimer’s Disease

by Dr. Michael Lee – Health Editor

Can Honey Protect Your Brain?⁢ Study Reviews Its Potential Against Alzheimer’s

A recent ‌review ​of laboratory studies suggests honey may offer ​a surprising defense against alzheimer’s ⁣Disease ⁢(AD).Published in Nutrients in 2025, the research, led by M.D. Navarro-Hortal and colleagues,‍ examined a range⁤ of experiments – from⁢ those ⁣using isolated cells to studies involving invertebrates like the ⁤nematode‌ Caenorhabditis elegans and the ⁣fruit ‍fly Drosophila melanogaster, as ⁤well as rodent models – to understand ⁤how different ​types ‍of honey impact AD pathology. The review⁢ considered the diverse sources and types of honey, ⁢including Manuka, Tualang,​ Chestnut, and Avocado varieties.

The findings indicate‌ honey combats several⁢ key hallmarks of AD, including oxidative stress,⁢ inflammation, ⁤and ⁤neurotransmitter imbalances. Researchers found honey and its extracts⁤ significantly reduced levels⁣ of ⁣reactive oxygen species (ROS),⁤ damaging molecules linked to cellular harm,⁤ in various models.

For example, chestnut-derived honey demonstrated antioxidative activity by protecting neuronal ‍cells from glutamate-induced damage and preserving mitochondrial function at concentrations between 500 and 750 ⁣μg/mL. In C. elegans engineered to produce human amyloid-beta, both Manuka and avocado honey⁤ (at 100 mg/mL) notably delayed the onset of ‌paralysis ⁤caused by Aβ. This suggests‍ a ⁣potent ⁢anti-inflammatory and anti-Aβ efficacy. Interestingly, the study also revealed a paradoxical effect: in some worm models of tauopathy, honey ⁢ worsened mobility, perhaps due ⁣to its sugar content rather than a direct impact on tau.

These findings were further supported by experiments using murine models. Tualang honey reversed shifts‍ in hippocampal Aβ1-40 and ⁢Aβ1-42 levels ⁢induced by LPS, while ​Kelulut honey reduced ⁣Aβ1-42 deposition ​specifically in the dentate gyrus, but not in‍ the CA1 or CA3 regions of the‌ brain. Furthermore, certain⁢ honeys exhibited the ability to inhibit ‍acetylcholinesterase, the⁢ enzyme ​responsible for breaking down acetylcholine – a ‍neurotransmitter crucial for memory. Acetylcholinesterase inhibitors are⁤ currently used as symptomatic treatments ‌for AD.However, the review authors caution that results ⁤varied significantly depending on the honey type, botanical source, processing methods, and study design. They also noted⁢ that many of the included studies ​carried a high or unclear risk of ⁤bias.

The review concludes that, in laboratory​ and non-human models, honey demonstrates meaningful neuroprotective ⁤potential, triggering benefits against the molecular drivers of AD by ‌reducing oxidative stress and inflammation and interfering with‍ toxic protein ​aggregation. Despite these⁣ promising results, ​the authors emphasize a “stark lack⁤ of human-derived‌ 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-Márquez, J. M.,Ansary,J.,‍ Hinojosa-Nogueira, D., Montalbán-Hernández, C., varela-López, A., & Quiles, J.⁣ L. (2025). Honey⁣ as a Neuroprotective Agent: molecular Perspectives on ⁢Its Role in Alzheimer’s disease. Nutrients,⁢ 17(16), 2577. DOI – 10.3390/nu17162577. https://www.mdpi.com/2072-6643/17/16/2577

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