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Multiple Sclerosis, Alzheimer’s Disease, and Inflammation: A Hypothetical View

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Immunotoxicity, Immune Dysfunction, and Chronic Disease

Part of the book series: Molecular and Integrative Toxicology ((MOLECUL))

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Abstract

Neurodegenerative diseases share many common characteristics. In this chapter we will present current understanding of the genetic, immunologic, and environmental basis of multiple sclerosis (MS) and Alzheimer’s disease (AD). The etiology of AD and MS is not known, but one factor that is common to the pathogenesis of these diseases is inflammation. We will discuss the pathogenesis of the different types of mechanisms that environmental and genetic factors can impose on these diseases with special emphasis on inflammation or inflammatory responses.

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Abbreviations

AD:

Alzheimer’s disease

ApoE:

Apolipoprotein E

APP:

Amyloid precursor protein

ATP:

Adenosine triphosphate

BBB:

Blood–brain barrier

cAMP:

Cyclic adenosine monophosphate

CNS:

Central nervous system

CR:

Complement receptor

CSF:

Cerebrospinal fluid

DCs:

Dendritic cells

EAE:

Experimental autoimmune encephalomyelitis

EBV:

Epstein–Barr virus

GA:

Glatiramer acetate

HHV6:

Human herpes virus 6

HLA:

Human leukocyte antigen

HSV:

Herpes simplex virus

IBD:

Inflammatory bowel diseases

ICAM-1:

Intercellular adhesion molecule 1

IFN-β:

Interferon beta

IFN-γ:

Interferon gamma

IL:

Interleukin

IPEX:

Immune dysregulation, polyendocrinopathy, enteropathy, X-linked

LRP:

Lipoprotein receptor-related protein

MAC:

Membrane attack complex

MAG:

Myelin-associated glycoprotein

MBP:

Myelin basic protein

M-CSF:

Macrophage colony-stimulating factor

MHC:

Major histocompatibility complex

MOG:

Myelin oligodendrocyte glycoprotein

MS:

Multiple sclerosis

NO:

Nitric oxide

NSAIDs:

Non-steroidal anti-inflammatory drugs

NTFs:

Neurofibrillary tangles

PLP:

Proteolipid protein

RAGE:

Receptor for advanced glycation end products

TGF-β:

Transforming growth factor beta

Th:

T helper

TLRs:

Toll-like receptors

TNF-α:

Tumor necrosis factor alpha

VCAM1:

Vascular cell adhesion molecule 1

VLA4:

Very late antigen 4

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Acknowledgments

This work is funded by the National Institutes of Health Grant R01 NS063011 (To M.S.B.). I thank Michael Kaplan for technical assistance. CV is a CNRS investigator.

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Bynoe, M.S., Viret, C. (2012). Multiple Sclerosis, Alzheimer’s Disease, and Inflammation: A Hypothetical View. In: Dietert, R., Luebke, R. (eds) Immunotoxicity, Immune Dysfunction, and Chronic Disease. Molecular and Integrative Toxicology. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-61779-812-2_9

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