Ting-Ting Yang is the Professor in neuroscience in School of Medicine for international students and a senior fellow of School of Chinese Medicine for Post-Baccalaureate at I-Shou University. She has also been a visiting professor in the atomic bomb disease institute at Nagasaki University. Dr. Yang received master’s level training and doctoral training in cellular and molecular biology at Nagasaki University. The major focus of her ongoing research is the investigation of disease- and treatment-induced changes in gene and protein expression profiles that regulate neuroenergetics and neuroplasticity signaling pathways in Neurodegeneration Disease including Alzheimer's disease and Parkinson's disease et.al. She has received ongoing research funding from the above mentioned. As a scientist she has been a major contributor to progress in the field of neuroscience research for more than 17 years. In addition to research, Dr. Yang teaches neuropathology to B.S./ M.S. students of I-Shou University.
Microglial activation (MA) and dopaminergic (DA) neuron loss are features of aging brain in Parkinson’s disease (PD). Although the etiology of PD remains unclear, age and inflammation are known PD risk factors. Because reduced brain-derived neurotrophic factor (BDNF) are associated with DA neuron loss in the substantia nigra (SN), age- and LPS-related BDNF/TrkB Signaling Pathway for MA and DA neuron loss in PD have been characterized. Infusing recombinant BDNF into the SN of mice at 6-month-old by osmotic mini-pump for 3 months, we found BDNF inhibited LPS-evoked area of MA in SN, striatum, hippocampus. Exposure to LPS induced phosphorylation of p38, JNK, and GSK3, which then increased phosphorylation of NF-кB. Phosphorylated NF-кB translocated into nucleus and bound to CBP and other coactivators. The NF-кB-CBP complex then induced transcription of inflammatory-related genes. Exogenous supplement with BDNF or endogenous up-regulating the expression of BDNF by exercise inhibited MA. Potential suppressive mechanisms of BDNF on MA might depend on three pathways: 1) BDNF induced Erk activation, which then phosphorylates CREB. Activated CREB inhibited NF-κB activity through competition for limited amounts of CBP. Activated CREB was also known to induce transcription of anti-inflammatory genes. Furthermore, activated CREB might also induced a positive feed forward production of BDNF. 2) BDNF actives Akt, which inhibited the activation of GSK3, resulting in a decrease of NF-кB activation and an increase of CREB activation. 3) BDNF upregulated MKP-1, which then reduced the LPS-induced phosphorylation of p38 and JNK.
Mahboubeh Manouchehrabadi is a MS. c, student in Developmental Biology Islamic Azad University of Karaj. She is expert in experimenting in vitro and in vivo models of Parkinson’s disease. In this regard, she has studied the neuroprotective effect of phenolic monoterpene carvacrol in both models.
Parkinson's disease (PD) is a progressive neurodegenerative movement disorder characterized by selective loss of dopaminergic neurons and the presence of lewy bodies. Treatment for PD that prevents neuronal death in the dopaminergic system and abnormal protein deposition in the brain is not yet available. Evidence from human and animal studies has suggested that oxidative damage critically contributes to neuronal loss in PD. This study aimed to evaluate the potential neuroprotective effects of Carvacrol on PC12 cells treated with 6-OHDA, a cellular model of Parkinson's disease. Carvacrol, a naturally occurring monoterpenic phenol and food additive, has been shown to have antimicrobials, antitumor, neuroprotective and antidepressant – like activities. We found that Carvacrol protect against 6-OHDA induced cell death in a dose-dependent manner. Neuroprotection was found to coincide with increasing cell viability and reductions in intracellular reactive oxygen species and lipid peroxidation. This study demonstrate that Carvacrol protected against 6-OHDA induced cell death via inhibition of oxidative stress, suggesting that Carvacrol may be a candidate neuroprotective agent for 6-OHDA induced Parkinsonism, and possibly for other genetic or sporadic forms of PD.