Nikhil Prasad Fact checked by:Thailand Medical News Team Sep 20, 2026 47 minutes ago
A lipid extract from the anchoring structure of giant Patagonian kelp protected brain cells from several metabolic disruptions associated with Alzheimer’s disease in laboratory experiments, raising interest in marine compounds as potential sources of future neuroprotective treatments.
Patagonian giant kelp holdfast lipids protected neuronal glucose metabolism and energy balance from
amyloid-beta-related disruption in laboratory experiments
Researchers are from Universidad de Magallanes; Universidad de las Américas; Universidad San Sebastián; and the University of Texas McGovern Medical School at Houston.
Kelp extract protects vulnerable neurons
The study investigated Macrocystis pyrifera, a giant kelp abundant in southern Patagonia. Scientists compared lipid extracts from its fronds, stipes, and holdfasts—the root-like structures that anchor kelp to the seafloor. The extracts were tested at 0.1 micrograms per milliliter in primary mouse hippocampal neurons and acute hippocampal slices.
Amyloid-beta 1–42, a peptide closely associated with Alzheimer’s pathology, reduced neuronal viability by approximately 40%. The holdfast-derived lipid extract, known as LEFH, produced the strongest protective response, restoring viability to levels statistically indistinguishable from untreated controls.
Brain-cell energy metabolism was preserved
One of the most striking findings in this
Thailand Medical News report involved glucose metabolism. Amyloid-beta reduced neuronal glucose uptake by approximately 50%, while LEFH maintained uptake close to normal levels.
Amyloid-beta also reduced glycolysis from 0.63 to 0.35 pmol/mg protein. LEFH significantly limited this decline and preserved activity in the pentose phosphate pathway, another important route for glucose utilization and cellular defense.
Under basal conditions, LEFH increased intracellular glutathione to approximately 135% of control levels and glutathione peroxidase activity to roughly 130%. However, researchers emphasized that these experiments did not establish protection against amyloid-beta-induced oxidative stress.
LEFH also increased the cellular ATP/ADP ratio and more than doubled PGC-1α gene expression, while GLUT4 mRNA increased approximately threefold. These changes point toward effects on cellular energy regulation, although they do not prove corresponding increases in protein activity.
Findings extend beyond isolated cells
Importantly, similar effects appeared in mouse hippocampal slices. Amyloid-beta cut glucose uptake by approximately half and lowered cellular energy status, while LEFH significantly attenuated both effects.
Conclusions
The findings identify holdfast-derived kelp lipids as a promising experimental source of compounds capable of preserving neuronal energy metabolism during amyloid-beta stress. However, chemical characterization, mechanistic
studies, chronic animal experiments, and ultimately human research are required before any therapeutic relevance can be established.
The study findings were published in the peer reviewed journal: Pharmaceuticals.
https://www.mdpi.com/1424-8247/19/9/1489
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https://www.thailandmedical.news/articles/alzheimer,-dementia-
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