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The Role of Inflammation in Alzheimer's Disease

Permanent Link: http://ncf.sobek.ufl.edu/NCFE003901/00001

Material Information

Title: The Role of Inflammation in Alzheimer's Disease
Physical Description: Book
Language: English
Creator: Coons, Elizabeth M.
Publisher: New College of Florida
Place of Publication: Sarasota, Fla.
Creation Date: 2008
Publication Date: 2008

Subjects

Subjects / Keywords: Inflammation
Alzheimer's Disease
Neurodegeneration
Genre: bibliography   ( marcgt )
theses   ( marcgt )
government publication (state, provincial, terriorial, dependent)   ( marcgt )
born-digital   ( sobekcm )
Electronic Thesis or Dissertation

Notes

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.
Statement of Responsibility: by Elizabeth M. Coons
Thesis: Thesis (B.A.) -- New College of Florida, 2008
Electronic Access: RESTRICTED TO NCF STUDENTS, STAFF, FACULTY, AND ON-CAMPUS USE
Bibliography: Includes bibliographical references.
Source of Description: 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.
Local: Faculty Sponsor: Beulig, Alfred

Record Information

Source Institution: New College of Florida
Holding Location: New College of Florida
Rights Management: Applicable rights reserved.
Classification: local - S.T. 2008 C7
System ID: NCFE003901:00001

Permanent Link: http://ncf.sobek.ufl.edu/NCFE003901/00001

Material Information

Title: The Role of Inflammation in Alzheimer's Disease
Physical Description: Book
Language: English
Creator: Coons, Elizabeth M.
Publisher: New College of Florida
Place of Publication: Sarasota, Fla.
Creation Date: 2008
Publication Date: 2008

Subjects

Subjects / Keywords: Inflammation
Alzheimer's Disease
Neurodegeneration
Genre: bibliography   ( marcgt )
theses   ( marcgt )
government publication (state, provincial, terriorial, dependent)   ( marcgt )
born-digital   ( sobekcm )
Electronic Thesis or Dissertation

Notes

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.
Statement of Responsibility: by Elizabeth M. Coons
Thesis: Thesis (B.A.) -- New College of Florida, 2008
Electronic Access: RESTRICTED TO NCF STUDENTS, STAFF, FACULTY, AND ON-CAMPUS USE
Bibliography: Includes bibliographical references.
Source of Description: 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.
Local: Faculty Sponsor: Beulig, Alfred

Record Information

Source Institution: New College of Florida
Holding Location: New College of Florida
Rights Management: Applicable rights reserved.
Classification: local - S.T. 2008 C7
System ID: NCFE003901:00001

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