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  1. Article ; Online: Inflammation and anti-inflammatory strategies for Alzheimer's disease--a mini-review.

    McNaull, Benjamin Brian Alexander / Todd, Stephen / McGuinness, Bernadette / Passmore, Anthony Peter

    Gerontology

    2010  Volume 56, Issue 1, Page(s) 3–14

    Abstract: Until recently, the central nervous system (CNS) has been thought to be an immune privileged organ. However, it is now understood that neuroinflammation is linked with the development of several CNS diseases including late-onset Alzheimer's disease (LOAD) ...

    Abstract Until recently, the central nervous system (CNS) has been thought to be an immune privileged organ. However, it is now understood that neuroinflammation is linked with the development of several CNS diseases including late-onset Alzheimer's disease (LOAD). The development of inflammation is a complex process involving a wide array of molecular interactions which in the CNS remains to be further characterized. The development of neuroinflammation may represent an important link between the early stages of LOAD and its pathological outcome. It is proposed that risks for LOAD, which include genetic, biological and environmental factors can each contribute to impairment of normal CNS regulation and function. The links between risk factors and the development of neuroinflammation are numerous and involve many complex interactions which contribute to vascular compromise, oxidative stress and ultimately neuroinflammation. Once this cascade of events is initiated, the process of neuroinflammation can become overactivated resulting in further cellular damage and loss of neuronal function. Additionally, neuroinflammation has been associated with the formation of amyloid plaques and neurofibrillary tangles, the pathological hallmarks of LOAD. Increased levels of inflammatory markers have been correlated with an advanced cognitive impairment. Based on this knowledge, new therapies aimed at limiting onset of neuroinflammation could arrest or even reverse the development of the disease.
    MeSH term(s) Aged ; Alzheimer Disease/immunology ; Alzheimer Disease/therapy ; Encephalitis/immunology ; Encephalitis/therapy ; Humans ; Neuroimmunomodulation/immunology
    Language English
    Publishing date 2010
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 193798-4
    ISSN 1423-0003 ; 0304-324X
    ISSN (online) 1423-0003
    ISSN 0304-324X
    DOI 10.1159/000237873
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Inflammation and Anti-Inflammatory Strategies for Alzheimer’s Disease – A Mini-Review

    McNaull, Benjamin Brian Alexander / Todd, Stephen / McGuinness, Bernadette / Passmore, Anthony Peter

    Gerontology

    2009  Volume 56, Issue 1, Page(s) 3–14

    Abstract: Until recently, the central nervous system (CNS) has been thought to be an immune privileged organ. However, it is now understood that neuroinflammation is linked with the development of several CNS diseases including late-onset Alzheimer’s disease (LOAD) ...

    Institution Department of Geriatric Medicine, Queen’s University Belfast, Belfast, UK
    Abstract Until recently, the central nervous system (CNS) has been thought to be an immune privileged organ. However, it is now understood that neuroinflammation is linked with the development of several CNS diseases including late-onset Alzheimer’s disease (LOAD). The development of inflammation is a complex process involving a wide array of molecular interactions which in the CNS remains to be further characterized. The development of neuroinflammation may represent an important link between the early stages of LOAD and its pathological outcome. It is proposed that risks for LOAD, which include genetic, biological and environmental factors can each contribute to impairment of normal CNS regulation and function. The links between risk factors and the development of neuroinflammation are numerous and involve many complex interactions which contribute to vascular compromise, oxidative stress and ultimately neuroinflammation. Once this cascade of events is initiated, the process of neuroinflammation can become overactivated resulting in further cellular damage and loss of neuronal function. Additionally, neuroinflammation has been associated with the formation of amyloid plaques and neurofibrillary tangles, the pathological hallmarks of LOAD. Increased levels of inflammatory markers have been correlated with an advanced cognitive impairment. Based on this knowledge, new therapies aimed at limiting onset of neuroinflammation could arrest or even reverse the development of the disease.
    Keywords Late-onset Alzheimer’s disease ; Neuroinflammation
    Language English
    Publishing date 2009-09-10
    Publisher S. Karger AG
    Publishing place Basel, Switzerland
    Document type Article
    Note Clinical Section
    ZDB-ID 193798-4
    ISSN 1423-0003 ; 0304-324X
    ISSN (online) 1423-0003
    ISSN 0304-324X
    DOI 10.1159/000237873
    Database Karger publisher's database

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