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Cornel iridoid glycoside found to improve brain function by clearing tau oligomers and reducing neurotoxicity


In this study, Chinese researchers investigated the mechanisms behind the effects of cornel iridoid glycoside (CIG) on tau oligomers and cognitive function. Their results were published in the Journal of Natural Medicines.

  • Tau oligomers are said to be one of the main contributors to Alzheimer’s disease.
  • They correlate strongly with the loss of neurons since they are neurotoxic.
  • According to recent studies, small tau oligomers are the most relevant toxic aggregate species.
  • To evaluate the neuroprotective effects of CIG, the main active component of Cornus officinalis (Japanese cornel), the researchers injected wortmannin (WM) and GF-109203X (GFX) into the lateral ventricles of rats to induce tau oligomer formation and impair their memory.
  • They reported that memory-impaired rats given either 60 or 120 mg/kg CIG daily for 14 days performed much better in the Morris water maze test than untreated rats.
  • CIG also restored the expression of presynaptic p-synapsin, synaptophysin and postsynaptic density-95 (PSD-95), which have been reduced by WM/GFX treatment, in the rat cortex.
  • In addition, CIG reduced the accumulation of tau oligomers in the brain, as well as in cells transfected with wildtype glycogen synthase kinase-3B (wtGSK-3B).
  • CIG also increased the levels of autophagy-related genes (ATG7, ATG12, Beclin-1 and LC3II), suggesting that CIG can restore autophagy function.

Based on these findings, the researchers concluded that CIG from Japanese cornel can ameliorate memory deficits and regulate memory-associated synaptic proteins by clearing tau oligomers via the restoration of autophagy.

Journal Reference:

Yang C, Li X, Zhang L, Li Y, Li L, Zhang L. CORNEL IRIDOID GLYCOSIDE INDUCES AUTOPHAGY TO PROTECT AGAINST TAU OLIGOMER NEUROTOXICITY INDUCED BY THE ACTIVATION OF GLYCOGEN SYNTHASE KINASE-3?. Journal of Natural Medicines. 12 June 2019;73(4):717–726. DOI: 10.1007/s11418-019-01318-3

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