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Moniz D, Esteves R, Cardoso S, Oliviera C. 2009. Endoplasmic     Reticulum and Mitochondria interplay
mediates apoptotic cell death: Relevance To Parkinson’s Disease. Neurochemistry International
55: 341-348
Parkison Disease, a progressive neurodegenerative disease, can be related with the Endoplasmic
Reticulum Stress and dysfunction of the mitochondria in the dopaminergic neurotransmission cells. The
researches establish this hypothesis: the calcium is the mediator between the Endoplasmic Reticulum and
the 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 by
the mitochondria during the Cellular Respiration and the second is a fluorometric measurement of ER and
Mitochondria Calcium levels. The results of this research were that the hypothesis was true. They found
that 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 is
helpful to my review paper because is related with the apoptotic activity of the cell, Parkinson Disease
and the mitochondrial activity It also prove a relation between the mitochondrial activity and the
dopaminergic cells death.
Zhang J, Montine TJ, Smith MA, Siedlak SL, Gu G, Robertson D and Perry G. 2002. The mitochondrial
common deletion in Parkinson’s disease and related movement disorders. Parkinsonism and
Related Disorders 8:165-170
Mitochondrial 4977b deletion had proven to be related with the Parkinson Disease and the movement
disorders cause by the neurological system but there is a conflict between what caused the deletion of this
mtDNA: the aging or the PD itself. The researches are trying to prove that the deletion of this mtDNA is
caused by the nigral neurons of the patients that have PD. The process or methodology that they were
using was the use of insidious hybridization assay. The have a population of 47 PD patients. Finally they
found that the PD was not related with the Mitochondrial 4977b deletion. Furthermore, the aging in
conjunction with the PD was not the cause of the Deletion. They conclude that maybe the deletion it’s not
directly related with the PD. On the other hand they expressed that if this is right then it have to be that
the mutations are affecting the complexes of the mitochondria and this is affecting the apoptotic activity
of this neurotransmission cells. This Is helpful to my review paper principally because it’s explain a
debate that persist in the neuroscience realm that is the relation between the mutations of the
mitochondria and the Parkinson Disease.

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Annotated bibliography endoplasmic reticulum and mitochondria interplay mediates apoptotic cell death.docx

  • 1. Moniz D, Esteves R, Cardoso S, Oliviera C. 2009. Endoplasmic Reticulum and Mitochondria interplay mediates apoptotic cell death: Relevance To Parkinson’s Disease. Neurochemistry International 55: 341-348 Parkison Disease, a progressive neurodegenerative disease, can be related with the Endoplasmic Reticulum Stress and dysfunction of the mitochondria in the dopaminergic neurotransmission cells. The researches establish this hypothesis: the calcium is the mediator between the Endoplasmic Reticulum and the 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 by the mitochondria during the Cellular Respiration and the second is a fluorometric measurement of ER and Mitochondria Calcium levels. The results of this research were that the hypothesis was true. They found that 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 is helpful to my review paper because is related with the apoptotic activity of the cell, Parkinson Disease and the mitochondrial activity It also prove a relation between the mitochondrial activity and the dopaminergic cells death. Zhang J, Montine TJ, Smith MA, Siedlak SL, Gu G, Robertson D and Perry G. 2002. The mitochondrial common deletion in Parkinson’s disease and related movement disorders. Parkinsonism and Related Disorders 8:165-170 Mitochondrial 4977b deletion had proven to be related with the Parkinson Disease and the movement disorders cause by the neurological system but there is a conflict between what caused the deletion of this mtDNA: the aging or the PD itself. The researches are trying to prove that the deletion of this mtDNA is caused by the nigral neurons of the patients that have PD. The process or methodology that they were using was the use of insidious hybridization assay. The have a population of 47 PD patients. Finally they found that the PD was not related with the Mitochondrial 4977b deletion. Furthermore, the aging in conjunction with the PD was not the cause of the Deletion. They conclude that maybe the deletion it’s not directly related with the PD. On the other hand they expressed that if this is right then it have to be that the mutations are affecting the complexes of the mitochondria and this is affecting the apoptotic activity of this neurotransmission cells. This Is helpful to my review paper principally because it’s explain a debate that persist in the neuroscience realm that is the relation between the mutations of the mitochondria and the Parkinson Disease.