Implications of Neuroimmunity in Alzheimer’s Disease: A Review

AD is characterized cognitively by memory, problem-solving, and language difficulties. It is estimated that 5.4 million Americans currently have Alzheimer’s disease (AD). The cognitive difficulties in AD are reflected in the brain through the accumulation of amyloid-β (Aβ) in cerebral amyloid angiop...

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Main Author: Katriel Lee
Format: Article
Language:English
Published: Appalachian State University Honors College 2017-10-01
Series:Impulse: The Premier Undergraduate Neuroscience Journal
Subjects:
Online Access:https://impulse.appstate.edu/sites/impulse.appstate.edu/files/Lee.2017.pdf
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spelling doaj-b0c94288cb764bb39195a3b705f64ea52020-11-25T00:04:54ZengAppalachian State University Honors CollegeImpulse: The Premier Undergraduate Neuroscience Journal1934-33611934-33612017-10-01Implications of Neuroimmunity in Alzheimer’s Disease: A ReviewKatriel Lee0Transylvania University, Lexington, Kentucky 40508AD is characterized cognitively by memory, problem-solving, and language difficulties. It is estimated that 5.4 million Americans currently have Alzheimer’s disease (AD). The cognitive difficulties in AD are reflected in the brain through the accumulation of amyloid-β (Aβ) in cerebral amyloid angiopathy (CAA), neurofibrillary tau tangles, neuronal tissue atrophy, and neuroinflammation, but the exact cause of AD is still in question. However, evidence suggests that differences in neuroimmune function—the central nervous system’s ability to resist disease—may play a role in the development and progression of AD. This paper largely relates neuroimmune changes to the amyloid hypothesis of AD. This approach relates AD to Aβ production and clearance, and therefore, targets Aβ for treatment uses. A thorough literature search revealed evidence that the blood-brain barrier (BBB), glial cell mediation and effects on neuroinflammation, and cerebrospinal fluid (CSF) and interstitial fluid (ISF) drainage systems are changed in AD. These changes seem to be detrimental for the AD brain and Aβ accumulation. Future research should be conducted regarding characterization of the lymphatic system in the human dura, the balance of helpful and harmful effects of activated microglia, the driving forces of paravascular CSF-ISF exchange, the effects of sleep on neuroimmunity, and genetic risk factors for neuroimmune dysfunction.https://impulse.appstate.edu/sites/impulse.appstate.edu/files/Lee.2017.pdfAlzheimer's DiseaseNeuroimmunity
collection DOAJ
language English
format Article
sources DOAJ
author Katriel Lee
spellingShingle Katriel Lee
Implications of Neuroimmunity in Alzheimer’s Disease: A Review
Impulse: The Premier Undergraduate Neuroscience Journal
Alzheimer's Disease
Neuroimmunity
author_facet Katriel Lee
author_sort Katriel Lee
title Implications of Neuroimmunity in Alzheimer’s Disease: A Review
title_short Implications of Neuroimmunity in Alzheimer’s Disease: A Review
title_full Implications of Neuroimmunity in Alzheimer’s Disease: A Review
title_fullStr Implications of Neuroimmunity in Alzheimer’s Disease: A Review
title_full_unstemmed Implications of Neuroimmunity in Alzheimer’s Disease: A Review
title_sort implications of neuroimmunity in alzheimer’s disease: a review
publisher Appalachian State University Honors College
series Impulse: The Premier Undergraduate Neuroscience Journal
issn 1934-3361
1934-3361
publishDate 2017-10-01
description AD is characterized cognitively by memory, problem-solving, and language difficulties. It is estimated that 5.4 million Americans currently have Alzheimer’s disease (AD). The cognitive difficulties in AD are reflected in the brain through the accumulation of amyloid-β (Aβ) in cerebral amyloid angiopathy (CAA), neurofibrillary tau tangles, neuronal tissue atrophy, and neuroinflammation, but the exact cause of AD is still in question. However, evidence suggests that differences in neuroimmune function—the central nervous system’s ability to resist disease—may play a role in the development and progression of AD. This paper largely relates neuroimmune changes to the amyloid hypothesis of AD. This approach relates AD to Aβ production and clearance, and therefore, targets Aβ for treatment uses. A thorough literature search revealed evidence that the blood-brain barrier (BBB), glial cell mediation and effects on neuroinflammation, and cerebrospinal fluid (CSF) and interstitial fluid (ISF) drainage systems are changed in AD. These changes seem to be detrimental for the AD brain and Aβ accumulation. Future research should be conducted regarding characterization of the lymphatic system in the human dura, the balance of helpful and harmful effects of activated microglia, the driving forces of paravascular CSF-ISF exchange, the effects of sleep on neuroimmunity, and genetic risk factors for neuroimmune dysfunction.
topic Alzheimer's Disease
Neuroimmunity
url https://impulse.appstate.edu/sites/impulse.appstate.edu/files/Lee.2017.pdf
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