Unraveling the neuroprotective mechanisms of elephant black garlic extract against beta amyloid peptide-induced neurotoxicity
Year: 2026
Type: article
Abstract: , this preparation exhibits a markedly different chemical profile enriched in sulfur-containing metabolites such as 3H-1,2-dithiol-3-thione (D3T) and 4-methyl-1,2,3-trithiolane (TTL). These compounds are rarely detected in traditional black garlic extracts and may underlie the specific protective effects observed in this study. Consequently, the biological actions described here cannot be generalized to other black garlic preparations. We provide the first evidence that Chilean Elephant Black Garlic (BG) confers neuroprotection against the toxicity of soluble oligomers of amyloid-beta (SO-Aβ), a central pathogenic element of Alzheimer's disease (AD) known to trigger synaptic dysfunction and mitochondrial impairment. In mouse hippocampal slices, BG prevented SO-Aβ-induced reductions in cell viability. Complementary experiments in cultured hippocampal neurons showed that BG preserved spontaneous calcium signaling and prevented SO-Aβ-mediated alterations in neuronal arborization. At the molecular level, BG restored the expression of synaptic proteins (SV2 and PSD-95) and maintained BDNF levels. Beyond synaptic protection, BG also preserved mitochondrial function under SO-Aβ challenge by maintaining mitochondrial membrane potential, intracellular ATP levels, and Mitofusin-1 expression. Altogether, these findings identify Chilean Elephant Black Garlic, as functional food, that represent an important source of bioactive compounds with properties capable of counteracting key neurotoxic mechanisms implicated in AD.
Source: Frontiers in Nutrition
Institution: University of Concepción
Language: English
Topic: Garlic and Onion Studies
Subfield: Plant Science
Domain: Life Sciences
Open Access status: gold
Estimated APC paid: $3,801
Awards: CONTRIBUTION OF GLYCINE RECEPTORS TO THE PATHOPHYSIOLOGY OF CHRONIC PAIN AND TO THE ANALGESIA INDUCED BY ALLOSTERIC MODULATORS NOVEL INSIGHTS COMING FROM BRAIN AND MIDBRAIN STRUCTURES WITHIN THE PAIN PATHWAY., THE OVEREXPRESSION OF P2X2 RECEPTORS ALTERS THE HIGH CA2+ MICRODOMAINS (HCMDS) LEADING TO INCREASED MITOCHONDRIA-ASSOCIATED ER MEMBRANES (MAMS) ABNORMAL APP PROCESSING AND VESICLE RECYCLING IN ALZHEIMER'S DISEASE MODELS.
OpenAlex ID: W7124438268
