Moniz D, Esteves R, Cardoso S, Oliviera C. 2009. Endoplasmic Reticulum and Mitochondria interplaymediates apoptotic cell death: Relevance To Parkinson’s Disease. Neurochemistry International55: 341-348Parkison Disease, a progressive neurodegenerative disease, can be related with the EndoplasmicReticulum Stress and dysfunction of the mitochondria in the dopaminergic neurotransmission cells. Theresearches establish this hypothesis: the calcium is the mediator between the Endoplasmic Reticulum andthe Mitochondria crosstalk causing a series of signal that is traduce by the cell in apoptosis (Cell Death).To prove this they use two principal methods: the first is to indentify how much NADH is synthesizes bythe mitochondria during the Cellular Respiration and the second is a fluorometric measurement of ER andMitochondria Calcium levels. The results of this research were that the hypothesis was true. They foundthat when MPP+ (neurotoxin) increase, the activity or the mitochondria decrease causing the apoptosis.Also they discovered a wide relation between the calcium and the mitochondria apoptotic activity. This ishelpful to my review paper because is related with the apoptotic activity of the cell, Parkinson Diseaseand the mitochondrial activity It also prove a relation between the mitochondrial activity and thedopaminergic cells death.Zhang J, Montine TJ, Smith MA, Siedlak SL, Gu G, Robertson D and Perry G. 2002. The mitochondrialcommon deletion in Parkinson’s disease and related movement disorders. Parkinsonism andRelated Disorders 8:165-170Mitochondrial 4977b deletion had proven to be related with the Parkinson Disease and the movementdisorders cause by the neurological system but there is a conflict between what caused the deletion of thismtDNA: the aging or the PD itself. The researches are trying to prove that the deletion of this mtDNA iscaused by the nigral neurons of the patients that have PD. The process or methodology that they wereusing was the use of insidious hybridization assay. The have a population of 47 PD patients. Finally theyfound that the PD was not related with the Mitochondrial 4977b deletion. Furthermore, the aging inconjunction with the PD was not the cause of the Deletion. They conclude that maybe the deletion it’s notdirectly related with the PD. On the other hand they expressed that if this is right then it have to be thatthe mutations are affecting the complexes of the mitochondria and this is affecting the apoptotic activityof this neurotransmission cells. This Is helpful to my review paper principally because it’s explain adebate that persist in the neuroscience realm that is the relation between the mutations of themitochondria and the Parkinson Disease.