ISBN-13: 9781632411945 / Angielski / Twarda / 2015 / 216 str.
ISBN-13: 9781632411945 / Angielski / Twarda / 2015 / 216 str.
Various therapeutic modalities and treatments of Parkinson's disease (PD) have been described in this book. This disease is caused mainly due to the death of dopaminergic neurons in the substantia nigra. Recent PD medications treat symptoms; though none decrease the rate of dopaminergic neuron degeneration. The primary problem in development of neuroprotective therapies is a restricted comprehension of the crucial molecular mechanisms that incite neurodegeneration. The discovery of PD genes has led to the hypothesis that dysfunction of the ubiquitin-proteasome pathway and misfolding of proteins are both critical to pathogenesis of the disease. Oxidative stress and mitochondrial dysfunction, earlier labeled as responsible in the neurodegeneration of this disease, may also act in part by causing the collection of misfolded proteins, along with the production of other harmful events in dopaminergic neurons. PD models based on the manipulation of PD genes should prove crucial in explaining significant characteristics of the disease, like selective vulnerability of substantia nigra dopaminergic neurons to the degenerative process. Some important topics include theoretical model for PD, PD in drosophila, animal models of PD, etc.
Various therapeutic modalities and treatments of Parkinsons disease (PD) have been described in this book. This disease is caused mainly due to the death of dopaminergic neurons in the substantia nigra. Recent PD medications treat symptoms; though none decrease the rate of dopaminergic neuron degeneration. The primary problem in development of neuroprotective therapies is a restricted comprehension of the crucial molecular mechanisms that incite neurodegeneration. The discovery of PD genes has led to the hypothesis that dysfunction of the ubiquitin-proteasome pathway and misfolding of proteins are both critical to pathogenesis of the disease. Oxidative stress and mitochondrial dysfunction, earlier labeled as responsible in the neurodegeneration of this disease, may also act in part by causing the collection of misfolded proteins, along with the production of other harmful events in dopaminergic neurons. PD models based on the manipulation of PD genes should prove crucial in explaining significant characteristics of the disease, like selective vulnerability of substantia nigra dopaminergic neurons to the degenerative process. Some important topics include theoretical model for PD, PD in drosophila, animal models of PD, etc.