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      Non-Steroidal Anti-Inflammatory Drugs in Alzheimer's Disease and Parkinson's Disease: Reconsidering the Role of Neuroinflammation

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          Abstract

          Alzheimer's disease (AD) and Parkinson's disease (PD) are the most common neurodegenerative diseases with age as the greatest risk factor. As the general population experiences extended life span, preparation for the prevention and treatment of these and other age-associated neurological diseases are warranted. Since epidemiological studies suggested that non-steroidal anti-inflammatory drug (NSAID) use decreased risk for AD and PD, increasing attention has been devoted to understanding the costs and benefits of the innate neuroinflammatory response to functional recovery following pathology onset. This review will provide a general overview on the role of neuroinflammation in these neurodegenerative diseases and an update on NSAID treatment in recent experimental animal models, epidemiological analyses, and clinical trials.

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          Most cited references185

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          Inhibition of prostaglandin synthesis as a mechanism of action for aspirin-like drugs.

          J R Vane (1971)
          Article 0 comments Cited 641 times – based on 0 reviews     Review now
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            Inflammation and Alzheimer's disease.

            H Akiyama, S. Barger, S Barnum … (2000)
            Inflammation clearly occurs in pathologically vulnerable regions of the Alzheimer's disease (AD) brain, and it does so with the full complexity of local peripheral inflammatory responses. In the periphery, degenerating tissue and the deposition of highly insoluble abnormal materials are classical stimulants of inflammation. Likewise, in the AD brain damaged neurons and neurites and highly insoluble amyloid beta peptide deposits and neurofibrillary tangles provide obvious stimuli for inflammation. Because these stimuli are discrete, microlocalized, and present from early preclinical to terminal stages of AD, local upregulation of complement, cytokines, acute phase reactants, and other inflammatory mediators is also discrete, microlocalized, and chronic. Cumulated over many years, direct and bystander damage from AD inflammatory mechanisms is likely to significantly exacerbate the very pathogenic processes that gave rise to it. Thus, animal models and clinical studies, although still in their infancy, strongly suggest that AD inflammation significantly contributes to AD pathogenesis. By better understanding AD inflammatory and immunoregulatory processes, it should be possible to develop anti-inflammatory approaches that may not cure AD but will likely help slow the progression or delay the onset of this devastating disorder.
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              The role of apolipoprotein E in Alzheimer's disease.

              Jungsu Kim, Jacob Basak, David Holtzman (2009)
              The epsilon4 allele of apolipoprotein E (APOE) is the major genetic risk factor for Alzheimer's disease (AD). Although there have been numerous studies attempting to elucidate the underlying mechanism for this increased risk, how apoE4 influences AD onset and progression has yet to be proven. However, prevailing evidence suggests that the differential effects of apoE isoforms on Abeta aggregation and clearance play the major role in AD pathogenesis. Other potential mechanisms, such as the differential modulation of neurotoxicity and tau phosphorylation by apoE isoforms as well as its role in synaptic plasticity and neuroinflammation, have not been ruled out. Inconsistent results among studies have made it difficult to define whether the APOE epsilon4 allele represents a gain of toxic function, a loss of neuroprotective function, or both. Therapeutic strategies based on apoE propose to reduce the toxic effects of apoE4 or to restore the physiological, protective functions of apoE.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Pharmaceuticals (Basel)
                Journal ID (iso-abbrev): Pharmaceuticals (Basel)
                Journal ID (publisher-id): pharmaceuticals
                Title: Pharmaceuticals
                Publisher: MDPI
                ISSN (Electronic): 1424-8247
                Publication date (Electronic): 02 June 2010
                Publication date Collection: June 2010
                Volume: 3
                Issue: 6
                Pages: 1812-1841
                Affiliations
                Department of Biology, Carleton College, one north college street, Northfield, MN 55057, USA
                Author notes
                [* ]Author to whom correspondence should be addressed; E-Mail: amoore@ 123456carleton.edu ; Tel.: +1-507-222-5981; Fax: +1-507-222-5757.
                Article
                Publisher ID: pharmaceuticals-03-01812
                DOI: 10.3390/ph3061812
                PMC ID: 4033954
                PubMed ID: 27713331
                SO-VID: 8a54eff3-263e-41a7-9ae2-718b5d69305c
                Copyright © © 2010 by the authors; licensee MDPI, Basel, Switzerland.
                License:

                This article is an Open Access article distributed under the terms and conditions of the Creative Commons Attribution license ( http://creativecommons.org/licenses/by/3.0/).

                History
                Date received : 08 April 2010
                Date revision received : 10 May 2010
                Date accepted : 02 June 2010
                Categories
                Subject: Review

                Keywords: non-steroidal anti-inflammatory drugs,alzheimer's disease,parkinson's disease,cyclooxygenase,neuroinflammation
                Data availability:
                Keywords: non-steroidal anti-inflammatory drugs, alzheimer's disease, parkinson's disease, cyclooxygenase, neuroinflammation

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