Alzheimer’s disease as an inflammatory disease

Bolós, Marta; Perea, Juan Ramón; Ávila, Jesús

doi:10.1515/bmc-2016-0029

Cited by 177 publications

(129 citation statements)

References 90 publications

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“…Numerous studies have established the role of neuroinflammation in both AD and PD pathology [28,96]. When inflammation is activated, neurones, and microglia cells release pro-inflammatory mediators (e.g., cytokines) which can stimulate an inflammatory response which damages neuronal cells and ultimately brain tissue [97,98].…”

Section: Discussionmentioning

confidence: 99%

Exposure to Environmental and Occupational Particulate Air Pollution as a Potential Contributor to Neurodegeneration and Diabetes: A Systematic Review of Epidemiological Research

Dimakakou

Johnston

Streftaris

et al. 2018

IJERPH

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It has been hypothesised that environmental air pollution, especially airborne particles, is a risk factor for type 2 diabetes mellitus (T2DM) and neurodegenerative conditions. However, epidemiological evidence is inconsistent and has not been previously evaluated as part of a systematic review. Our objectives were to carry out a systematic review of the epidemiological evidence on the association between long-term exposure to ambient air pollution and T2DM and neurodegenerative diseases in adults and to identify if workplace exposures to particles are associated with an increased risk of T2DM and neurodegenerative diseases. Assessment of the quality of the evidence was carried out using the GRADE system, which considers the quality of the studies, consistency, directness, effect size, and publication bias. Available evidence indicates a consistent positive association between ambient air pollution and both T2DM and neurodegeneration risk, such as dementia and a general decline in cognition. However, corresponding evidence for workplace exposures are lacking. Further research is required to identify the link and mechanisms associated with particulate exposure and disease pathogenesis and to investigate the risks in occupational populations. Additional steps are needed to reduce air pollution levels and possibly also in the workplace environment to decrease the incidence of T2DM and cognitive decline.

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Section: Discussionmentioning

confidence: 99%

Exposure to Environmental and Occupational Particulate Air Pollution as a Potential Contributor to Neurodegeneration and Diabetes: A Systematic Review of Epidemiological Research

Dimakakou

Johnston

Streftaris

et al. 2018

IJERPH

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“…Excessive soluble and aggregated Aβ peptides and hyper-phosphorylation of tau protein stimulate plaque formation and structural/functional alterations of neurons in brain [4]. These deleterious alterations are reported to be accompanied by increased oxidative stress as well as pro-inflammatory response [56]. …”

Section: Introductionmentioning

confidence: 99%

Nicotinamide Reduces Amyloid Precursor Protein and Presenilin 1 in Brain Tissues of Amyloid Beta-Tail Vein Injected Mice

Kim

Yang

2017

Clin Nutr Res

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The purpose of this study is to investigate whether nicotinic acid (NA) and nicotinamide (NAM) reduce the Alzheimer disease (AD)-related gene expression in brain tissues of amyloid beta (Aβ)-injected mice. Male Crj:CD1 (ICR) mice were divided into 6 treatment groups; 1) control, 2) Aβ control, 3) Aβ + NA 20 mg/kg/day (NA20), 4) Aβ + NA40, 5) Aβ + NAM 200 mg/kg/day (NAM200), and 6) Aβ + NAM400. After 1-week acclimation period, the mice orally received NA or NAM once a day for a total of 7 successive days. On day 7, biotinylated Aβ42 was injected into mouse tail vein. At 5 hours after the injection, blood and tissues were collected. Aβ42 injection was confirmed by Western blot analysis of Aβ42 protein in brain tissue. NAM400 pre-treatment significantly reduced the gene expression of amyloid precursor protein and presenilin 1 in brain tissues. And, NAM200 and NAM400 pre-treatments significantly increased sirtuin 1 expression in brain tissues, which is accompanied by the decreased brain expression of nuclear factor kappa B by 2 doses of NAM. Increased expression of AD-related genes was attenuated by the NAM treatment, which suggests that NAM supplementation may be a potential preventive strategy against AD-related deleterious changes.

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“…AD-associated inlammation is generally considered as a secondary response to the pathological lesions evoked by Aβ [35,36]. AD-related inlammatory response is supposed to be driven mainly by activated microglia [37,38].…”

Section: Ad-related Neuroinlammationmentioning

confidence: 99%

Interleukin 1 Receptor and Alzheimer’s Disease-Related Neuroinflammation

Wang¹,

Wang²

2017

Mechanisms of Neuroinflammation

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Neuroinlammation as one of the pathogenic mechanisms concerning to the development of Alzheimer's disease (AD) has aroused more atention since last decades. Amyloid beta (Aβ) peptide generation is supposed to be the initial event in AD progress, followed by neuronal impairment, neuroinlammation, and severe substantial neuronal dysfunction. Interleukin-1 receptor (IL-1R) as one of the most prevalent inlammatory mediated surface receptors, participates not only in peripheral inlammation but also in AD-related neuroinlammation. In microglia, IL-1R activation triggers the downstream signaling and the production of proinlammatory cytokines and chemokines. IL-1R signaling also participates in AD-related Aβ-induced inlammasome activation. Besides, IL-1R activation in neurons may increase APP non-amyloid pathway by modulation of APP α-secretase activity, which may prevent neurotoxic Aβ generation. Thus, the exact role of IL-1R signaling in AD development and neuronal functions is somehow tricky.

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Alzheimer’s disease as an inflammatory disease

Cited by 177 publications

References 90 publications

Exposure to Environmental and Occupational Particulate Air Pollution as a Potential Contributor to Neurodegeneration and Diabetes: A Systematic Review of Epidemiological Research

Exposure to Environmental and Occupational Particulate Air Pollution as a Potential Contributor to Neurodegeneration and Diabetes: A Systematic Review of Epidemiological Research

Nicotinamide Reduces Amyloid Precursor Protein and Presenilin 1 in Brain Tissues of Amyloid Beta-Tail Vein Injected Mice

Interleukin 1 Receptor and Alzheimer’s Disease-Related Neuroinflammation

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