The Role of Inflammation in Alzheimer's Disease

Date of Award

2008

Document Type

Thesis

Degree Name

Bachelors

Department

Natural Sciences

First Advisor

Beulig, Alfred

Keywords

Inflammation, Alzheimer's Disease, Neurodegeneration

Area of Concentration

Biological Psychology

Abstract

Alzheimer�s Disease (AD) is the number one cause of dementia. As the baby boomer generation ages, the number of cases will increase and health care costs will continue to rise. Current treatments that exist for AD are only moderately successful at slowing disease progression, therefore; it is important to learn more about the etiology and pathology of AD. Immune up-regulation is thought to contribute to AD etiology and progression via interactions with senile plaques. Inflammatory substances such as a-chymotrypsin, C-reactive protein, and complement fragments surround plaques. Complement fragments, such as C1b, have been shown to bind to and increase the formation of AB42. Yet, blocking complement and cytokine production has been shown to increase plaque formation. These results have given rise to a new theory, the immune dysfunction theory, which states that AD results not from immune up-regulation, but rather from the functional inability of the immune system to effectively prevent disease. Activated microglia and astrocytes, the CNS immune cells, have also been linked to neurodegeneration. They have been observed surrounding neuronal plaques. When activated by AB42, they release inflammatory cytokines and neurotoxins, which may contribute to neurodegeneration. Yet they are also necessary for the removal of AB42 from neuronal plaques, a process that is inhibited in vivo. Ineffective microglial phagocytosis has been linked to AB-induced physical changes. Recent studies have shown that blood-derived microglia may be necessary for the effective removal of AB from neuronal plaques.

Rights

This bibliographic record is available under the Creative Commons CC0 public domain dedication. The New College of Florida, as creator of this bibliographic record, has waived all rights to it worldwide under copyright law, including all related and neighboring rights, to the extent allowed by law.

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