The pathogenesis of neurodegenerative disorders by Mark P. Mattson

By Mark P. Mattson

During this groundbreaking publication, best specialists element the mobile and molecular cascades that reason selective degeneration of neuronal populations, and remove darkness from these genetic and environmental elements which are severe to the facilitation or suppression of the neuropathologic strategies. operating from reviews of human sufferers, in addition to from mobilephone tradition and animal versions, the authors display a heretofore unrecognized convergence of the causative pathogenetic mechanisms for clinically specified neurological problems. At heart level are the biochemical and molecular cascades that might eventually result in neuronal death-cascades regarding oxyradical construction, aberrant law of mobile ion homeostasis, activation of particular proteases, and activation of a stereotyped series of occasions related to mitochondial disorder. person chapters research how those mechanisms-along with genetic and environmental factors-operate in Alzheimer's and Parkinson's illnesses, Down's syndrome, amyotropic lateral sclerosis, ischemic stroke, spinal wire damage, and Duchenne muscular dystrophy.

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The brain also contains a small amount of catalase (CAT). Numerous other nonenzymatic antioxidants and metal chelators are present in the brain. Neurodegenerative Diseases 23 Table 1 Antioxidants Enzymatic Nonenzymatic Copper–zinc superoxide dismutase Manganese superoxide dismutase Catalase Glutathione peroxidase Glutathione reductase Alpha and gamma tocopherol Ascorbic acid Ceruloplasmin Uric acid Bilirubin Melatonin Glutathione Methionine Antioxidant-defense mechanisms can be upregulated in response to increased freeradical production (Cohen and Werner, 1994).

1994) demonstrated that aggregated amyloid (A`)-peptides are capable of generating free radicals and inducing oxidative events. Dyrks et al. (1992) showed that an in vitro iron-catalyzed oxidation system caused transformation of nonaggregated A`-peptides into aggregated forms. , 1995) and antioxidants are capable of preventing experimental A`-peptide-induced neuron death in cultured cells (Goodman and Mattson, 1994; Mattson, 1997). , 1998), which can produce ONOO–. Thus, it is possible that the increase in aggregated A`-peptides in the brain in AD may increase free radical production that could play a role in its neurotoxicity.

J. Cereb. Blood Flow Metab. 18, 180–185. Senut, M. , Suhr, S. , and Gage, F. H. (2000) Intraneuronal aggregate formation and cell death after viral expression of expanded polyglutamine tracts in the adult rat brain. J. Neurosci. 20, 219–229. , Perri, B. , Trojanowski, J. , Flamm, E. , and McIntosh, T. K. (1997) Improvement of cognitive deficits and decreased cholinergic neuronal cell loss and apoptotic cell death following neurotrophin infusion after experimental traumatic brain injury. J. Neurosurg.

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