Alzheimer’s Disease, Inflammation, and the Role of Antioxidants
Open accessAbstract
The World Health Organization refers to Alzheimer’s disease (AD) as a global health priority. As the average age of the world’s population is increasing, so too is the rate of AD. There are an estimated 47 million people globally who have been diagnosed with AD dementia, and researchers have yet to figure out the root cause. All misfolded aggregate proteins that are involved in neurodegenerative disorders (amyloid-β, Huntington’s tau, α-synuclein) induce oxidative stress. It is that oxidative stress that leads to inflammation and, in conjunction with amyloid protein and tau hyperphosphorylation, progresses to and exacerbates AD. The consumption of antioxidants and nutrients, specifically vitamin E, caffeine, and turmeric, may slow the progression of AD and can be found in a wide variety of dietary foods. This review explores the role of inflammation on AD, the antioxidants that can potentially combat it, and future directions of how the treatment of the disease can be better understood.
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Persistent activation of microglia may result in failure to resolve inflammation, contributing to neuronal damage and cognitive decline associated with AD.
“The persistent activation of microglia may result in a failure to resolve inflammation, contributing to neuronal damage and the cognitive decline associated with AD [15,16].”
From Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease (2024) · cites this paper as [15]
Various pathological factors, such as Aβ plaques, pro-inflammatory cytokines, and oxidative stress, activate microglia, leading to release of pro-inflammatory mediators that exacerbate neurotoxicity.
“This hypothesis posits that various pathological factors, such as Aβ plaques, pro-inflammatory cytokines, and oxidative stress, activate microglia, the central nervous system’s innate immune cells. Upon activation, microglia undergo morphological changes and initiate a variety of inflammatory responses, which can lead to the release of pro-inflammatory mediators that exacerbate neurotoxicity.”
From Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease (2024) · cites this paper as [15]
The inflammatory hypothesis suggests that chronic neuroinflammation plays a significant role in the pathogenesis of AD.
“The inflammatory hypothesis suggests that chronic neuroinflammation plays a significant role in the pathogenesis of AD.”
From Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease (2024) · cites this paper as [15]
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“AD is rapidly becoming one of the world’s most serious cognitive diseases (Sinyor et al. 2020).”
BackgroundThe Breakthroughs and Caveats of Using Human Pluripotent Stem Cells in Modeling Alzheimer’s Disease
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“Antioxidants such as Vitamin E, caffeine, and turmeric have been well acknowledged as potentially having an impact on delaying disease progression or disease onset [90].”
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“However, there are various hypotheses regarding the development of AD such as involvement of Aβamyloid, Tau, the formation of neurofibrillary tangles, degeneration of cholinergic neurons, inflammation, and oxidative stress [1].”
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“Antioxidants are both endogenous and exogenous molecules that limit the detrimental effects of free radicals in neuronal cells through detoxification [8].”
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Lipoprotein-Associated Phospholipase A2 Is a Risk Factor for Patients With Parkinson’s Disease
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“Current researches show that inflammation has become a common cause of many neurodegenerative diseases, such as Alzheimer’s disease (AD; Sinyor et al., 2020), dementia (Peila and Launer, 2006), amyotrophic lateral sclerosis (McCauley and Baloh, 2019), and Huntington’s disease (Pac et al.”
BackgroundNanomodulators That Target Alzheimer’s Disease: A Review
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Chronic Stress as a Risk Factor for Type 2 Diabetes: Endocrine, Metabolic, and Immune Implications
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“…peripheral disorders [3,8,9] with significant involvement of reactive oxygen species and the anti-oxidative system, inflammation, obesity, and hypertension as determining factors [9,10], and the trajectory of comorbidity could be different from that of the aging population without AD symptoms [11].”
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Epigenetic modifications of DNA and RNA in Alzheimer’s disease
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“Exposure to heavy metals or air pollutants, diets low in antioxidants, physical inactivity, comorbidities, and social factors can increase the risk of AD (Chen et al., 2016; Cacciottolo et al., 2017; Sinyor et al., 2020).”
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“Proinflammatory cytokines (e.g., TNF, IL-1, and IL-6) are upregulated in the brains of persons with AD, suggesting inflammation is a hallmark contributor to AD development (Sinyor et al., 2020).”
InfluentialAn Open Question: Is the A2A Adenosine Receptor a Novel Target for Alzheimer’s Disease Treatment?
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“Finally, recent works support the utility of caffeine intake as antioxidant and antiinflammatory agent (Janitschke et al., 2019; Sinyor et al., 2020).”
BackgroundButyrylcholinesterase-inhibiting natural coumarin molecules as potential leads
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“Furthermore, high intake of vitamin E may be related to the decrease in the clinical progression of early Alzheimer's disease symptoms and with a lower occurrence of Alzheimer's disease (Sinyor et al., 2020). α-tocopherol–”
BackgroundSideritis scardica Extracts Demonstrate Neuroprotective Activity against Aβ25–35 Toxicity
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Nanoparticles-based delivery system and its potentials in treating central nervous system disorders
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“Studies have suggested that CNS inflammation can be caused by CNS disorders such as AD and PD [66, 67].”
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Beneficial Effects of Sideritis clandestina Extracts and Sideridiol against Amyloid β Toxicity
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“Various studies have suggested the lower probability of AD onset and progression upon consumption of antioxidants [19–21].”
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“Antioxidant properties in the drug design for Alzheimer’s disease have become desirable due to the oxidative stress underlying the pathology and progression of this devastating disease [40].”
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“21,36,37 32-34 32-34 research suggests that there is potential for therapeutics for Alzheimer’s disease Healthy brains of mice and humans have populations of brain resident CD69 Tregs, and these have been shown to expand rapidly in several neuroinflammatory conditions.”
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“Thus, researchers have suggested that antioxidants play the role in delaying the progression of dementia (Sinyor et al., 2020).”
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Potential drugs for the treatment of Alzheimer’s disease
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“Resveratrol possesses strong antioxidant activity that contributes to the reduction of NF-κβ activity [65, 104].”
BackgroundCan Porphyromonas gingivalis Contribute to Alzheimer’s Disease Already at the Stage of Gingivitis?
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“This initiate accumulation of amyloid- (A ) plaques and tau hyperphosphorylation (hallmarks of AD) which cause loss of neurons [39].”
BackgroundWięckowski, K., Szałaj, N., Gryzło, B., Wichur, T., Góral, I., Sługocka, E., Śniecikowska, J., Latacz, G., Siwek, A., Godyń, J., et al. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23169443 · Cited by 8 · see citing works
“One of the mechanisms by which antioxidants reduce the concentration of ROS and therefore prevent or slow the cell damage caused by free radicals is scavenging them [53].”
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“Inflammation and AD are inevitably linked, with more research needed to solidify the mechanisms associated with them, including the intake of antioxidants for a healthier life [11].”
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“Abnormal aggregation of neurotoxic Aβ promotes inflammatory responses, oxidative stress, and apoptotic activation, which results in extensive neuron death and the onset of clinical symptoms [26].”
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“As such, it may be beneficial to encourage the consumption of foods that are rich in vitamin E, such as nuts, seeds, vegetable oils, and green leafy vegetables [37].”
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Exploring the Neuroprotective Effects of Rufinamide in a Streptozotocin-Induced Dementia Model
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“In this condition, pro-inflammatory cytokines such as TNF-α, IL-1β, NF-κB, and IL-6 are elevated in the brain leading to the accumulation of Aβ plaques and tau hyperphosphorylation, and ultimately results in neuronal death (Sinyor et al. 2020).”
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“Thus, modulating Ach levels or inhibiting AChE could represent a potential treatment for AD (Sinyor et al., 2020).”
The Different Molecular Targets and Its Significant Role in Alzheimer’s Disease: A Review
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Effect of the aggregation state of amyloid-beta (25-35) on the brain oxidative stress in vivo
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Chaperones as Potential Pharmacological Targets for Treating Protein Aggregation Illness
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“Neuroinflammation contributes to the development and exacerbation of AD [3,6,7], PD [8] and other neurodegenerative disorders [9].”
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“, while in vitro or in vivo studies have demonstrated that antioxidants rich nutrients can protect the brain from oxidative damage, there are limited data about epidemiological and clinical trial studies; however, the evidence suggests that antioxidants could reduce the risk of inflammatory events that lead to AD prog…”
BackgroundCombinatorial therapy in Alzheimer's disease
Giri, M. A., Kendre, P. N., Bhalke, R. D., Pande, V. V., Autade, K. A., & Sumbe, R. B. (2024) · Elsevier eBooks · doi:10.1016/b978-0-443-13205-6.00026-1 · Cited by 4 · see citing works
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“Oxidative stress also contributes to the existence of the toxic peptide β-amyloid in the brain (Sinyor et al. 2020; Tamagno et al. 2021) Therefore, strategies for the treatment of AD have involved the use of antioxidants (Pritam et al. 2022).”
BackgroundVitamin E and cognitive function: A systematic review of clinical evidence
Amin, A. M., & Mostafa, H. M. A. (2025) · Nutrition Research · doi:10.1016/j.nutres.2025.11.009 · Cited by 4 · see citing works
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Guarana (Paullinia cupana Kunth): Applications to Alzheimer's disease and dementias
Arantes, L. P., Zamberlan, D. C., Machado, M. L., & Soares, F. A. A. (2023) · Elsevier eBooks · doi:10.1016/b978-0-323-90052-2.00021-4 · Cited by 3 · see citing works
Chemical Characterization and Assessment of the Neuroprotective Potential of Euphrasia officinalis
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Konsumsi Kopi untuk Mencegah Penyakit Alzheimer
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“Microglial activation and neuroinflammation, through the secretion of pro-inflammatory cytokines, also contribute to the process of neuronal destruction [41].”
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“Senile plaques show a toxic activity that exacerbates both the inflamma - tory response (Sinyor et al. 2020), leading to an increase in inflammatory cytokines, such as IL-1β (Liu et al. 2014a, b; Sinyor et al. 2020) and oxidative stress process (Calsolaro and Edison 2016 ), which, together,…”
InfluentialHalim, M. B. A., Metwally, G. F., Abd‐Elrazek, A., Al-Karmalawy, A. A., El-Zoheiry, H. H., Deeb, K. S. E., & Eid, H. H. (2024) · Scientific African · doi:10.1016/j.sciaf.2024.e02501 · Cited by 2 · see citing works
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“AD is another CNS disease closely associated with neuroinflammation; it is also closely related to various pathological factors including A β plaques, phosphorylated tau, proinflammatory cytokines, and oxidative stress, which can activate microglia and induce neuroinflammation (15, 16).”
Kahil, E. A., Jackson, A., D’Souza, B., Gorman, G. S., & Jumbo‐Lucioni, P. P. (2025) · Natural Product Research · doi:10.1080/14786419.2025.2477226 · Cited by 1 · see citing works
“In AD, microglia are commonly described in an activated state in response to Aβ accumulation in the brain (Sinyor et al. 2020).”
Malarte, M., Chiotis, K., Ioannou, K., & Rodriguez‐Vieitez, E. (2025) · Journal of Neurochemistry · doi:10.1111/jnc.70222 · Cited by 2 · see citing works
“…role of inflammation in the pathogenesis of AD could consist of either promoting or delaying disease progression through the dual pro-and anti-inflammatory states of microglia/astrocytes and their secreted cytokines and chemokines (Hickman et al. 2018; Kumar et al. 2023; Sinyor et al. 2020).”
Singh, V., Anamika, A., Chandra, N., Gupta, V., Gautam, P., Rath, S., Sethi, A. K., Chaurasia, R. N., & Mishra, V. N. (2025) · Elsevier eBooks · doi:10.1016/b978-0-443-36295-8.00001-8 · Cited by 1 · see citing works
- Authors
- Sinyor, B., Mineo, J., & Ochner, C.
- Affiliations
- HCA Healthcare (US)
- Corresponding author
- Sinyor, Benjamin
- Venue
- Journal of Alzheimer s Disease Reports
- Publisher
- SAGE Publications
- Published
- 2020-05-30
- Volume
- 4
- Issue
- 1
- Pages
- 175-183
- ISSN
- 2542-4823 (ISSN-L)
- PMC
- PMC7369138
- OpenAlex
- W3033403703
- Cited by
- 120
- References
- 58
- Citations by year
- 2026: 14 · 2025: 16 · 2024: 23 · 2023: 23 · 2022: 23 · 2021: 19 · 2020: 2
- FWCI
- 2.14
- Type
- journal article
- Language
- en
- Open access
- diamond
- doi.org
- Licence
- Locations
- Journal of Alzheimer s Disease Reports (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- HCA Healthcare
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- Alzheimer's disease, neuroinflammation, oxidative stress, antioxidants, amyloid-beta, tau hyperphosphorylation, protein aggregation, vitamin E, caffeine, turmeric, dietary nutrients, neurodegeneration
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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