Amyotrophic lateral sclerosis apoptosis

The lack of zinc can also be a problem in biological systems and is responsible for disease states. For example, nitric oxide-dependent apoptosis can be induced in motor neurons by zinc-deficient SOD, and in some cases of amyotrophic lateral sclerosis, zinc-deficient SOD may participate in this type of oxidative mechanism involving nitric oxide.969 One form of hereditary human hair loss or alopecia was mapped to a specific gene and a mutation found in affected individuals. The gene encodes a single zinc finger transcription factor protein with restricted expression in the brain and skin.970 Zinc has been implicated in Alzheimer s via beta amyloid formation, and a role has been attributed for the cerebral zinc metabolism in the neuropathogenesis of Alzheimer s disease.971... 

Martin, L. J. Neuronal death in amyotrophic lateral sclerosis is apoptosis possible contribution of a programmed cell death mechanism. /. Neuropathol. Exp. Neurol. 58 459-471, 1999. 

Sathasivam, S., Ince, P. G. and Shaw, P. I. Apoptosis in amyotrophic lateral sclerosis a review of the evidence. Neuropathol. Appl. Neurobiol. 27 257-274,2001. 

The pathological characteristic of Parkinson s disease is the selective degeneration of dopamine neurons in the pars compacta of the substantia nigra. The mechanism for the loss of neurons remains to be elucidated, and recently apoptosis has been proposed as a death process in Parkinson s disease. For example, the level of a product of the oxidative stress, 4-hydroxy-2-nonenal protein adduct, was found to increase in the nigral neurons of parkinsonian brains. Peroxynitrite (see Figure 13.6) has been proposed to be involved in the neuronal cell death in some neurodegenerative diseases, such as amyotrophic lateral sclerosis. 

Yoshihara T, Ishigaki S, Yamamoto M, Liang Y, Niwa J, Takeuchi H, et al. Differential expression of inflammation- and apoptosis-related genes in spinal cords of a mutant SOD1 transgenic mouse model of familial amyotrophic lateral sclerosis. J Neurochem 2002 80(1) 158—167. 

Abnormalities in cell death regulation can be a significant component of diseases such as cancer, autoimmune lymphoproliferative syndrome, AIDS, ischemia, and neurodegenerative diseases such as Parkinson s disease, Alzheimer s disease, Huntington s disease, and amyotrophic lateral sclerosis. Some conditions feature insufficient apoptosis, whereas others feature excessive apoptosis. 

Keywords Alzheimer s disease Amyotrophic lateral sclerosis Animal models Apoptosis Huntington s disease Neurodegeneration Neuroprotection Parkinson s disease Randomized controlled trials Therapeutics... 

Hensley K, Eloyd RA, Gordon B, Mon S, Pye QN, Stewart C, West M, Williamson K (2002) Temporal patterns of cytokine and apoptosis-related gene expression in spinal cords of the G93A-SOD1 mouse model of amyotrophic lateral sclerosis. J Neurochem 82 365-374. 

AID AIDP AIDS AIF AIRE AIS AES AMAN AMN AMPA AMSAN activation-induced (cytidine) deaminase acute inflammatory demyelinating polyradiculoneuropathy acquired immunodeficiency syndrome apoptosis inducing factor autoimmune regulator anterior chamber associated immune deviation (ACAID)-inducing signal amyotrophic lateral sclerosis acute motor axonal neuropathy adrenomyeloneuropathy a-amino-3 -hydroxy-5-methylisoxazole- 4-propionic acid acute motor-sensory axonal neuropathy... 

Part III Chaps. 9-13) describes the application ofimmnnocytochemical techniques to the study of other very important areas of current research in the neurosciences such as apoptosis/autophagy (Chap. 9), Alzheimer s disease (Chap. 10), amyotrophic lateral sclerosis (Chap. 11), microglia (Chap. 12), and the blood-brain barrier (Chap. 13). 

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