MicroRNA 221 rescues the loss of dopamine... - Cure Parkinson's
MicroRNA 221 rescues the loss of dopaminergic neurons in a mouse model of Parkinson's disease
Regulating miRNA by Natural Agents as a New Strategy for Cancer Treatment
ncbi.nlm.nih.gov/pmc/articl...
Natural agents including curcumin, isoflavone, I3C, DIM, EGCG, and resveratrol can impact on the expression levels of miRNAs and thereby lead to the inhibition of cancer cell growth along with induction of apoptosis and reversal of EMT to MET.
The Parkinson's disease gene product DJ-1 modulates miR-221 to promote neuronal survival against oxidative stress
sciencedirect.com/science/a....
DJ-1 protein can be a potential biomarker and therapeutic target for Parkinson's disease.
7. Diagnostic and therapeutic potency of DJ-1 in PD
The accuracy of the clinical diagnosis in the early stages of PD is still limited. Functional neuroimaging techniques are helpful in patients with first signs of parkinsonism, but are expensive and not broadly available. Therefore, a priority for the scientific community is the detection of PD pathology at early stages of the disease. In this regard, a recent study found that the ratio of neural-derived exosomal DJ-1 levels to total DJ-1 was increased in PD patients versus controls, and a positive correlation was found between levels of DJ-1 and α-Synuclein in plasma neural-derived exosomes, thus indicating a potential for exosomal DJ-1 as a PD biomarker [75]. Another study found that detection of DJ-1 in the cerebrospinal fluid can be used as a biomarker for PD [76], however, this potential of DJ-1 as a biomarker is still unclear, and larger clinical trials are needed to fully validate DJ-1 as a reliable PD biomarker.
DJ-1 has been found to be therapeutically effective for animal models of neurodegenerative disorders [77]. In some of these studies, rat PD models were tested for the efficacy of recombinant wild type DJ-1 for protection of dopaminergic neurons [78, 79]. Other studies adopted a novel strategy for obtaining DJ-1-mediated dopaminergic neuronal protection by preventing its overoxidation and thereby its inactivation [80]. By using brain penetrant molecules able to interact with the Cys106 region of DJ-1 that help DJ-1 maintain its active form, it was found that these DJ-1 interactors prevented dopaminergic neuronal death and restored normal locomotor function in rodent models of PD [81, 82]. These and other animal studies have explored DJ-1 as a possible therapeutic target for PD and neurodegeneration, however, such studies using human cohorts are currently missing and need to be undertaken that would represent an important step in unravelling the potential of DJ-1 as an ideal target for therapeutic intervention.