This drove our attention to unravel the possible involvement of PI3k/Akt/mTOR pathway in the neuroprotective effect of crocin against rotenone (ROT)-induced PD in rats.
To explore its possible mechanism in PD, we used 6-hydroxydopamine (6-OHDA, 8 μg) to mimic dopaminergic (DA) neuronal damage and validated this model in vivo and in vitro. in vivo, we detected an effect of PC (60 mg/kg) on the behavioural changes exhibited in 6-OHDA model rats, the number of DA neurons and the phosphorylation of protein kinase B (Akt). in vitro, we detected changes in cell viability, mitochondrial membrane potential (MMP) and total superoxide dismutase (SOD) and explored the role of PC (50 μM) by inhibiting the phosphoinositide 3-kinase (PI3K)/Akt signalling pathway with LY294002 (20 μM).
Effect of Vasicinone against Paraquat-Induced MAPK/p53-Mediated Apoptosis via the IGF-1R/PI3K/AKT Pathway in a Parkinson's Disease-Associated SH-SY5Y Cell Model.
Results showed that TMAS treatment elevated the levels of BDNF, cAMP response element-binding protein (CREB), and protein kinase B (p-Akt) in the PD model mouse hippocampus, but not in the non-PD mouse hippocampus.
Farrerol protects dopaminergic neurons in a rat model of lipopolysaccharide-induced Parkinson's disease by suppressing the activation of the AKT and NF-κB signaling pathways.
Lentiviral Vector-Mediated SHC3 Silencing Exacerbates Oxidative Stress Injury in Nigral Dopamine Neurons by Regulating the PI3K-AKT-FoxO Signaling Pathway in Rats with Parkinson's Disease.
A significant decrease in nuclear PI3K p85, Akt1/2/3 and PIP3 levels and significant increase in nuclear PTEN and GSK3β levels were observed in SN region of PD brain when compared to the age-matched controls.
Furthermore, PLD treatment significantly increased levels of p-AKT, p-GSK-3β<sup>Ser9</sup>, and Nrf2, and suppressed the activation of NF-κB in the SN of rats with LPS-induced PD.
We aim to investigate the effect of miR-181b on autophagy, particularly the involvement of miR-181b in the regulation of the phosphatase and tensin homolog (PTEN)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) pathway and neuronal autophagy in a 1-methyl-4- phenylpyridinium iodide(MPP<sup>+</sup>)-induced cellular model of Parkinson's disease.
Regulation of various signalling (Ras-MAPK, PI3K and AKT) pathways by augmented activity of neurotrophic factors (NTFs) could prevent or halt the progress of dopaminergic loss in Parkinson's disease (PD).
These results suggest that polymorphism of AKT1 locus is associated with risk of PD and that the G allele at rs2498799 may decrease the risk of PD in the North-eastern part of Han Chinese female population.
LRRK2 directly phosphorylates Akt1 as a possible physiological substrate: impairment of the kinase activity by Parkinson's disease-associated mutations.
In contrast to previously published results, our data do not support the hypothesis of genetic variants in AKT1 confering protection against Parkinson's disease.
The data presented here suggest the involvement of AKT1 in protection of PD through many possible mechanisms involving different signaling pathways that could be potential therapeutic targets in the future.