Neurodegenerative disorders are among the most devastating illnesses in western society. The disorders are chronic and progressive. Although these diseases are relatively common and often highly debilitating, the mechanisms responsible for their pathologies are poorly understood, and there are currently no effective preventative therapies. Over the past decade, many genes underlying heritable forms of the neurodegenerative disorders have been identified, including Alzheimer's disease, Parkinson's disease, Huntington’s Disease and Friedreich’s ataxia. Genetic anormalies that cause the neurodegenerative disorders are varied and complex. The disorders are characterized by the selective and symmetric loss of neurons in sensory, motor and cognitive systems. The challenge is to understand the pathogeneis of the neurogenerative disorders. There must be an understanding of the abnormalities in proteins transport, interaction and aggregation,

The outline of the patterns of cell loss and the identification of disease specific cell markers help in nosologic classification. Alzheimer’s disease is marked by senile plaques, neurofibrillary tangles, neuronal loss and t

Other motor neuron disorders are also inherited. Amyotrophic lateral sclerosis is an autosomal dominant trait that is characterized with spinal cord atrophy and muscles innervated. The cause of the motor neuron loss is unknown. Spinal muscular atrophy is an autosomal recessive disorder of childhood. Two genes of 5q13 are associated with the disorder. One gene encodes the survival motor neuron gene. Because of the deletion of the gene, 95 percent of patients have spinal muscular atrophy. There are also short deletions or missense mutations.

Studies done on understanding the pathogenesis of Alzheimer’s disease report that several genes have been identified with patients. Beta-amyloid-42 has been linked with families with familiar early onset of the disease. Seven different mutations in the gene for the amyloid precursor protein has been found to increase the making of beta amyloid 1- 42, leading to fibrillar aggregation toxic to neurons. A second locus linked early onset cases has been found on chromosome 14q and encodes a presenilin 1. More than 50 mutations in the gene for presenilin 1 has been found in people with early onset of the disease. Mutations in the presenilin genes and in the amyloid precursor protein are associated with the increased celllular production of the beta amyloid. Also the apoE gene on chromosome 19 has three common forms: e2, e3 and e4. Each one produces a corresponding form of apolipoprotein E. The presence of the e4 allele sets up the mechanism for the production of E4 form of apoE, which is t

Some topics in this essay:
Disease Friedreich’s, Alzeimer’s Parkinson’s, Disorders Neurodegenerative, parkinson’s disease, alzheimer’s disease, huntington’s disease, autosomal dominant, neurodegenerative disorders, mutations gene, lewy bodies, motor neuron, neurofibrillary tangles, parkinson’s disease lewy, amyotrophic lateral sclerosis, spinal muscular atrophy, alzeimer’s parkinson’s disease, disease lewy, senile plaques neurofibrillary,