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      Innate immunity in Alzheimer's disease.

      Author(s): 1 , 2 , 3
      Publication date (Electronic):
      Journal: Nature immunology

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          Abstract

          Alzheimer's disease (AD) is the world's most common dementing illness, affecting over 150 million patients. Classically AD has been viewed as a neurodegenerative disease of the elderly, characterized by the extracellular deposition of misfolded amyloid-β (Aβ) peptide and the intracellular formation of neurofibrillary tangles. Only recently has neuroinflammation emerged as an important component of AD pathology. Experimental, genetic and epidemiological data now indicate a crucial role for activation of the innate immune system as a disease-promoting factor. The sustained formation and deposition of Aβ aggregates causes chronic activation of the immune system and disturbance of microglial clearance functions. Here we review advances in the molecular understanding of the inflammatory response in AD that point to novel therapeutic approaches for the treatment of this devastating disease.

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          The genetics of Alzheimer disease: back to the future.

          Lars Bertram, Christina Lill, Rudolph E. Tanzi (2010)
          Three decades of genetic research in Alzheimer disease (AD) have substantially broadened our understanding of the pathogenetic mechanisms leading to neurodegeneration and dementia. Positional cloning led to the identification of rare, disease-causing mutations in APP, PSEN1, and PSEN2 causing early-onset familial AD, followed by the discovery of APOE as the single most important risk factor for late-onset AD. Recent genome-wide association approaches have delivered several additional AD susceptibility loci that are common in the general population, but exert only very small risk effects. As a result, a large proportion of the heritability of AD continues to remain unexplained by the currently known disease genes. It seems likely that much of this "missing heritability" may be accounted for by rare sequence variants, which, owing to recent advances in high-throughput sequencing technologies, can now be assessed in unprecedented detail. Copyright © 2010 Elsevier Inc. All rights reserved.
          Article 0 comments Cited 234 times – based on 0 reviews     Review now
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            CD33 Alzheimer’s disease locus: Altered monocyte function and amyloid biology

            Elizabeth Bradshaw, Lori B. Chibnik, Brendan T Keenan … (2013)
            In our functional dissection of the CD33 Alzheimer’s disease susceptibility locus, we find that the rs3865444C risk allele is associated with greater cell surface expression of CD33 in monocytes (t 50 = 10.06, pjoint=1.3×10–13) of young and older individuals. It is also associated with (1) diminished internalization of Aβ42) (2) accumulation of neuritic amyloid pathology and fibrillar amyloid on in vivo imaging and (3), increased numbers of activated human microglia.
            Article 0 comments Cited 230 times – based on 0 reviews     Review now
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              Nonsteroidal antiinflammatory drugs and the risk of Alzheimer's disease.

              Bas In 't Veld, Annemieke Ruitenberg, Albert Hofman … (2001)
              Previous studies have suggested that the use of nonsteroidal antiinflammatory drugs (NSAIDs) may help to prevent Alzheimer's disease. The results, however, are inconsistent. We studied the association between the use of NSAIDs and Alzheimer's disease and vascular dementia in a prospective, population-based cohort study of 6989 subjects 55 years of age or older who were free of dementia at base line, in 1991. To detect new cases of dementia, follow-up screening was performed in 1993 and 1994 and again in 1997 through 1999. The risk of Alzheimer's disease was estimated in relation to the use of NSAIDs as documented in pharmacy records. We defined four mutually exclusive categories of use: nonuse, short-term use (1 month or less of cumulative use), intermediate-term use (more than 1 but less than 24 months of cumulative use), and long-term use (24 months or more of cumulative use). Adjustments were made by Cox regression analysis for age, sex, education, smoking status, and the use or nonuse of salicylates, histamine Hz-receptor antagonists, antihypertensive agents, and hypoglycemic agents. During an average follow-up period of 6.8 years, dementia developed in 394 subjects, of whom 293 had Alzheimer's disease, 56 vascular dementia, and 45 other types of dementia. The relative risk of Alzheimer's disease was 0.95 (95 percent confidence interval, 0.70 to 1.29) in subjects with short-term use of NSAIDs, 0.83 (95 percent confidence interval, 0.62 to 1.11) in those with intermediate-term use, and 0.20 (95 percent confidence interval, 0.05 to 0.83) in those with long-term use. The risk did not vary according to age. The use of NSAIDs was not associated with a reduction in the risk of vascular dementia. The long-term use of NSAIDs may protect against Alzheimer's disease but not against vascular dementia.
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                Author and article information

                Journal
                Journal ID (iso-abbrev): Nat. Immunol.
                Title: Nature immunology
                ISSN (Electronic): 1529-2916
                ISSN (Print): 1529-2908
                Publication date (Electronic): Mar 2015
                Volume: 16
                Issue: 3
                Affiliations
                [1 ] 1] Clinical Neuroscience, Department of Neurology, University of Bonn, Bonn, Germany. [2] Department of Medicine, Division of Infectious Diseases and Immunology, University of Massachusetts Medical School, Worcester, Massachusetts, USA. [3] German Center for Neurodegenerative Diseases, Bonn, Germany.
                [2 ] Department of Medicine, Division of Infectious Diseases and Immunology, University of Massachusetts Medical School, Worcester, Massachusetts, USA.
                [3 ] 1] Department of Medicine, Division of Infectious Diseases and Immunology, University of Massachusetts Medical School, Worcester, Massachusetts, USA. [2] German Center for Neurodegenerative Diseases, Bonn, Germany. [3] Institute of Innate Immunology, University of Bonn, Bonn, Germany.
                Article
                Publisher Item ID: ni.3102
                DOI: 10.1038/ni.3102
                PubMed ID: 25689443
                SO-VID: f430b3ee-0a99-4bf7-8eef-484bfbfc6a1f
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