The DOI matches its Crossref record; 210 of the 210 references it cites were found in a registry or an index.
Anti-inflammatory and Immune Therapy for Alzheimers Disease: Current Status and Future Directions
Open accessAbstract
From the initial characterizations of inflammatory responses in Alzheimer's disease (AD) affected brains, namely the demonstration of activated microglia and reactive astrocytes, complement system activation, increased production of proinflammatory cytokines, and evidence for microglial-produced neurotoxins, there was hope that reducing inflammation might be a feasible treatment for this memory-robbing disease. This hope was supported by a number of epidemiology studies demonstrating that patients who took non-steroidal anti-inflammatory drugs had significantly lower risk of developing AD. However, clinical trials of anti-inflammatories have not shown effectiveness, and in recent years, the concept of immune therapy has become a treatment option as animal studies and clinical trials with Abeta vaccines have demonstrated enhanced amyloid removal through stimulation of microglial phagocytosis.This review will examine the current status of whether inhibiting inflammation is a valid therapeutic target for treating AD; what lessons have come from the clinical trials; what new pathways and classes of agents are being considered; and how this field of research can progress towards new therapeutics. We will examine a number of agents that have shown effectiveness in reducing inflammation amongst other demonstrated mechanisms of action. The major focus of much AD drug discovery has been in identifying agents that have anti-amyloid properties; however, a number of these agents were first identified for their anti-inflammatory properties. As drug development and clinical testing is a costly and lengthy endeavor, sound justification of new therapeutic targets is required. Possible future directions for AD anti-inflammatory or immune clearance therapy will be discussed based on recent experimental data.
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“In the past, clinical trials with various NSAIDs and glucocortoroids failed to rescue cognitive deficits in AD patients or prevent disease progression despite promising data from preclinical animal studies [186].”
From Glial contributions to neurodegeneration in tauopathies (2017) · cites this paper as [186]
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“Phytochemicals’ activity against AD occurred through different mechanisms such as their anti-amyloid, anticholinesterase, anti-inflammatory, and antioxidant properties [198].”
From Multi-Target Mechanisms of Phytochemicals in Alzheimer’s Disease: Effects on Oxidative Stress, Neuroinflammation and Protein Aggregation (2022) · cites this paper as [198]
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Metadata
- Authors
- Walker, D., & Lue, L.-F.
- Affiliations
- Banner Sun Health Research Institute (US)
- Corresponding author
- Walker, Douglas
- Venue
- Current Neuropharmacology
- Publisher
- Bentham Science Publishers Ltd.
- Published
- 2007-12-01
- Volume
- 5
- Issue
- 4
- Pages
- 232-243
- ISSN
- 1570-159X (ISSN-L)
- PMC
- PMC2644496
- OpenAlex
- W2031392840
- Cited by
- 66
- References
- 210
- Citations by year
- 2026: 1 · 2025: 2 · 2023: 7 · 2022: 5 · 2021: 9 · 2020: 7 · 2019: 5 · 2018: 3 · 2017: 4 · 2016: 3 · 2015: 3 · 2014: 1 · 2013: 1 · 2012: 1
- FWCI
- 2.23
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Current Neuropharmacology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- Alzheimer's Association
- National Institutes of Health
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- Alzheimer's disease, neuroinflammation, anti-inflammatory therapy, immunotherapy, microglia, reactive astrocytes, complement system, inflammatory cytokines, nonsteroidal anti-inflammatory drugs, amyloid clearance, microglial phagocytosis, anti-amyloid drugs, therapeutic target
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