Garlic-Derived Allicin Attenuates Parkinson's Disease via PKA/p-CREB/BDNF/DAT Pathway Activation and Apoptotic Inhibition.
Level 5 - mechanism / opinion, no new human data
Preclinical in vitro and animal research without human participants.
PubMed 40807441 · doi:10.3390/molecules30153265
What was done
The authors used bioinformatics and network pharmacology to predict potential therapeutic targets of allicin in Parkinson's disease. They evaluated these predictions experimentally using an in vitro 6-hydroxydopamine (6-OHDA) cytotoxicity model in SH-SY5Y cells and an in vivo 6-OHDA-induced Parkinson's disease mouse model. Key outcomes assessed included motor function, dopaminergic neuron loss, apoptosis markers (BAX, Bcl-2), and signaling pathway components (PKA, p-CREB, BDNF, DAT).
What was found
Allicin administration reduced 6-OHDA-induced cytotoxicity in SH-SY5Y cells and mitigated motor deficits and dopaminergic neuron loss in mice. Mechanistically, allicin increased brain dopamine transporter (DAT) levels, activated the PKA/p-CREB/BDNF pathway, modulated BAX and Bcl-2 expression, and suppressed neuronal apoptosis. The abstract reports no numerical values, effect sizes, or statistical figures.
Why it matters
This study outlines a plausible molecular mechanism—PKA/p-CREB/BDNF/DAT pathway activation—through which garlic-derived allicin may exert neuroprotective effects in neurodegenerative models.
Limits
The study is restricted to cell culture and a toxin-induced mouse model, which do not capture the full complexity and chronicity of human Parkinson's disease. The abstract does not disclose sample sizes, treatment dosages, effect sizes, or blood-brain barrier pharmacokinetics.
Cited by
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