Allergic rhinitis, bronchial asthma and other allergies in patients with Alzheimer’s disease: unnoticed issue

Bożek, Andrzej; Bednarski, Piotr; Jarząb, Jerzy

doi:10.5114/ada.2016.62842

Cited by 10 publications

(8 citation statements)

References 18 publications

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“…One-fifth of patients with AD have allergic diseases, such as bronchial asthma, atopic dermatitis, seasonal AR, perennial AR, and polymorphous atopic disease, and require treatment in Polish rural and urban areas [20]. In addition, 17.7% of patients with AD that have AR require treatment [24]. Expression of proinflammatory mediators, such as interleukin-18, immunoglobulin G, immunoglobulin M, and immunoglobulin E, result in AR in animal and human brain tissue and enhance the pathogenesis of AD [15,25,26].…”

Section: Discussionmentioning

confidence: 99%

Influence of PM2.5 Exposure Level on the Association between Alzheimer’s Disease and Allergic Rhinitis: A National Population-Based Cohort Study

Luo

et al. 2019

IJERPH

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Alzheimer’s disease (AD) is an irreversible neurodegenerative disease that leads to dementia, health impairment, and high economic cost. Allergic rhinitis (AR) is a chronic inflammatory and allergic disease of the respiratory system that leads to health problems and has major effects on the daily lives of patients and their caregivers. Particulate matter (PM) refers to air pollutants 2.5 μm or less in diameter that are a source of concern because of their role in numerous diseases, including AR and other neurodegenerative diseases. To date, no study has demonstrated how PM2.5 exacerbates AR and results in AD. We conducted a national population-based cohort study by obtaining patient data from the National Health Insurance Research Database of Taiwan for the 2008–2013 period. PM2.5 concentration data were obtained from the ambient air quality monitoring network established by the Environmental Protection Administration of Taiwan. Monthly PM2.5 exposure levels were categorized into quartiles from Q1–Q4. The Cox proportional hazards analysis, after adjusting for age, sex, low income, and urbanization level, revealed that patients with AR had an elevated risk of developing AD (hazard ratio (HR): 2.008). In addition, the cumulative incidence of AD in the AR group was significantly higher than in the comparison group. The PM2.5 levels at Q2–Q4 (crude HR: 1.663–8.315; adjusted HR: 1.812–8.981) were stratified on the basis of the PM2.5 exposure group and revealed that AR patients exposed to PM2.5 are significantly prone to develop AD. In addition, the logistic regression analyses, after adjustment, demonstrated that an increase in the PM2.5 exposure level at Q2–Q4 (adjusted odds ratio (OR): 2.656–5.604) increased the risk of AR in AD patients. In conclusion, an increased PM2.5 exposure level could be correlated with AR, which could in turn cause AD. AR increased the risk of AD, in which exposure to PM2.5 increases the higher probability of AD.

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Section: Discussionmentioning

confidence: 99%

Influence of PM2.5 Exposure Level on the Association between Alzheimer’s Disease and Allergic Rhinitis: A National Population-Based Cohort Study

Luo

et al. 2019

IJERPH

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“…Compared with individuals without allergies, those with all three allergic diseases had a substantially increased risk of AD (multivariable hazard ratios 1.46; 95% CI 1.25-1.70). Bo żek et al also noted a similar correlation between allergies and AD [97]. Conversely, allergies can exacerbate existing health issues for older adults with AD.…”

Section: Allergiesmentioning

confidence: 78%

Thirty Risk Factors for Alzheimer’s Disease Unified by a Common Neuroimmune–Neuroinflammation Mechanism

Weaver

2023

Brain Sciences

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One of the major obstacles confronting the formulation of a mechanistic understanding for Alzheimer’s disease (AD) is its immense complexity—a complexity that traverses the full structural and phenomenological spectrum, including molecular, macromolecular, cellular, neurological and behavioural processes. This complexity is reflected by the equally complex diversity of risk factors associated with AD. However, more than merely mirroring disease complexity, risk factors also provide fundamental insights into the aetiology and pathogenesis of AD as a neurodegenerative disorder since they are central to disease initiation and subsequent propagation. Based on a systematic literature assessment, this review identified 30 risk factors for AD and then extended the analysis to further identify neuroinflammation as a unifying mechanism present in all 30 risk factors. Although other mechanisms (e.g., vasculopathy, proteopathy) were present in multiple risk factors, dysfunction of the neuroimmune–neuroinflammation axis was uniquely central to all 30 identified risk factors. Though the nature of the neuroinflammatory involvement varied, the activation of microglia and the release of pro-inflammatory cytokines were a common pathway shared by all risk factors. This observation provides further evidence for the importance of immunopathic mechanisms in the aetiopathogenesis of AD.

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“…Furthermore, such factors recruit reactive microglia that can exacerbate inflammation by releasing proinflammatory cytokines such as TNF-a, IL-β, or IFNγ ( 47 ). Interestingly, clinical studies have shown that one fifth of diagnosed patients with AD have a history of allergies and chronic rhinitis that had required some sort of treatment ( 48 ). Such toxic factors not only cause neuronal damage directly but could also exacerbate ongoing pathological processes such as neuroinflammation ( 49 ) leading to further olfactory disturbances.…”

Section: Mechanisms Of the Olfactory Pathophysiology In Admentioning

confidence: 99%

Olfactory neuropathology in Alzheimer's disease: a sign of ongoing neurodegeneration

Son

Jahanshahi

Yoo

et al. 2021

BMB Rep

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Olfactory neuropathology is a cause of olfactory loss in Alzheimer's disease (AD). Olfactory dysfunction is also associated with memory and cognitive dysfunction and is an incidental finding of AD dementia. Here we review neuropathological research on the olfactory system in AD, considering both structural and functional evidence. Experimental and clinical findings identify olfactory dysfunction as an early indicator of AD. In keeping with this, amyloid-β production and neuroinflammation are related to underlying causes of impaired olfaction. Notably, physiological features of the spatial map in the olfactory system suggest the evidence of ongoing neurodegeneration. Our aim in this review is to examine olfactory pathology findings essential to identifying mechanisms of olfactory dysfunction in the development of AD in hopes of supporting investigations leading towards revealing potential diagnostic methods and causes of early pathogenesis in the olfactory system. [BMB Reports 2021; 54(6): 295-304]

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Allergic rhinitis, bronchial asthma and other allergies in patients with Alzheimer’s disease: unnoticed issue

Cited by 10 publications

References 18 publications

Influence of PM2.5 Exposure Level on the Association between Alzheimer’s Disease and Allergic Rhinitis: A National Population-Based Cohort Study

Influence of PM2.5 Exposure Level on the Association between Alzheimer’s Disease and Allergic Rhinitis: A National Population-Based Cohort Study

Thirty Risk Factors for Alzheimer’s Disease Unified by a Common Neuroimmune–Neuroinflammation Mechanism

Olfactory neuropathology in Alzheimer's disease: a sign of ongoing neurodegeneration

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