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Alzheimer's abstract

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Alzheimer's abstract Powered By Docstoc
					                                                                                                Brooke Wadlington
                                                                                                 Nut 313, Group #1
                                                                                                           4/11/11
                                           Abstract: Alzheimer’s Disease

Introduction

Alzheimer’s disease is main cause of dementia in older people. Pathological signs of the disease in the brain
include deposits of extracellular amyloid beta peptides in plaques containing elements of degenerating neurons,
intracellular deposits of abnormally hyperphosphorylated tau protein, loss of neurons and synapses, neurofibrillary
tangles, and loss of memory. There is no current cure for Alzheimer’s disease; however, there are preventative
measures.

Objective

The objective for this study is to state which nutritional vitamin and mineral help and prevent Alzheimer’s disease
from happening and/or worsening, and how the chosen vitamin and mineral works against the disease and the
problems it causes within the brain.

Materials and Methods

The vitamin and mineral chosen for this study was Copper and Vitamin E. Copper regulates amyloid precursor
protein (APP) expression. Accumulation of amyloid beta peptide (Aβ) is a major pathological feature of Alzheimer’s
disease and is generated from the cleavage of APP. Vitamin E has been shown to weaken degenerative factors
such as: inhibiting Aβ42 fibril formation, weakening Aβ42 induced neurotoxicity, disaggregating preformed fibrils,
interferring with Aβ oligomer formation, decreasing formation of reactive oxygen species and NO, and modulating
production of cytokines through the oxidized α-tocopherol, α-tocopherolquinone.

Results

An increase in exocytosis and a decrease in endocytosis suggests an increase in cell surface APP, which makes APP
important in copper homeostasis. Alzheimer’s disease requires α-tocopherolquinone to inhibit Aβ aggregation and
cytotoxicity, disaggregate preformed Aβ-peptide fibrils, and decrease formation of ROS and NO.

Summary and Discussion

Copper and Vitamin E, together, help and prevent AD from occurring and getting worse. More studies are needed
to establish the function of copper-responsive APP relocalization. Further studies should be done to test the
effectiveness of α-TQ at improving the memory and other AD pathologies.

References

Luchsinger JA, Mayeux R. Dietary factors and Alzheimer's disease. Lancet Neurol 2004;3:579–87.

Yang Shi-gao, Wang Wei-yun, Ling Tie-jun, Feng Ying, Du Xue-ting, Zhang Xi, Sun Xiao-xia, Zhao Min, Xue Di, Yang
Yang, Liu Rui-tian. Alpha-tocopherol quinone inhibits beta-amyloid aggregation and cytotoxicity, disaggregate
preformed fibrils and decreases the production of reactive oxygen species, NO and inflammatory cytokines.
Neurochemistry International 2010;57:914-922.

Acevedo Karla, Hung Ya Hui, Dalziel Andrew, Li Qiao-Xin, Laughton Katrina, Wikhe Krutika, Rembach Alan, Roberts
Blaine, Masters Colin, Bush Ashley, Camakaris James. Copper Promotes the Trafficking of the Amyloid Precursor
Protein. Journal of Biological Chemistry 2011;286:8252-8262.

				
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