Neuroinflammation: A Common Pathway in Alzheimer’s Disease and Epilepsy

Liew, Yee; Retinasamy, Thaarvena; Arulsamy, Alina; Ali, Idrish; Jones, Nigel C.; O’Brien, Terence J.; Shaikh, Mohd Farooq

doi:10.3233/jad-230059

Cited by 6 publications

(2 citation statements)

References 59 publications

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“…Neuroinflammation that is often associated with NIHL 81 is also a contributing factor to the initiation and advancement of Alzheimer's disease 82 . After exposure of rats to noise levels of 100dB for two hours daily during 15-and 30-days cognitive impairments were associated with elevated levels of TNF-α, IL-6, IL-1α, and IFN-γ in both hippocampus and plasma.…”

Section: Pathological Concepts Of Noise-ad Relationshipmentioning

confidence: 99%

Noise and Alzheimer's disease

Belojević

2023

Ann Nursing

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Alzheimer’s disease (AD) is the most common form of degenerative dementia and the seventh leading cause of death. Numerous influencing factors for AD have been investigated: aging, female gender, genetics, unhealthy diet, hearing loss, unhealthy lifestyle, physical inactivity, insufficient sleep, head injury, depression, hypertension, and environmental factors (air pollution, aluminum, silicon, selenium, pesticides, lack of sunbathing, electric and magnetic fields). Recent animal and human studies point to a possible relationship between noise exposure and AD. The aim of this narrative review is to present the basic pathological concepts of this relationship. Alzheimer’s disease (AD) is the most common form of degenerative dementia and the seventh leading cause of death. Numerous influencing factors for AD have been investigated: aging, female gender, genetics, unhealthy diet, hearing loss, unhealthy lifestyle, physical inactivity, insufficient sleep, head injury, depression, hypertension, and environmental factors (air pollution, aluminum, silicon, selenium, pesticides, lack of sunbathing, electric and magnetic fields). Recent animal and human studies point to a possible relationship between noise exposure and AD. The aim of this narrative review is to present the basic pathological concepts of this relationship. Possible mediating factors that explain the influence of noise on AD are sleep disturbance, excitotoxicity, oxidative stress injury in the auditory cortex and hippocampus, and systemic inflammation. Studies on animals point to cognitive dysfunctions related to noise exposure: anxiety-like behavior, impaired learning and memory, increased glutamate levels in the hippocampus, and reduced expression of N-methyl-D-aspartic acid receptor 2B. Neuropathological changes in animals exposed to noise include necrosis and apoptosis of hippocampal cells; accumulation of amyloid β; tau hyperphosphorylation and peroxidative damage in the hypothalamus and the auditory cortex; and elevated expression of proinflammatory cytokines and microglial activation in the auditory cortex and hippocampus. Human brain scan studies have pointed to the positive relationship between traffic noise exposure and white matter volume in the body of the corpus callosum at the level of the auditory cortex. In conclusion, there is a biological plausibility to the noise-AD relationship, and noise countermeasures may be regarded as the prevention of AD. Possible mediating factors that explain the influence of noise on AD are sleep disturbance, excitotoxicity, oxidative stress injury in the auditory cortex and hippocampus, and systemic inflammation. Studies on animals point to cognitive dysfunctions related to noise exposure: anxiety-like behavior, impaired learning and memory, increased glutamate levels in the hippocampus, and reduced expression of N-methyl-D-aspartic acid receptor 2B. Neuropathological changes in animals exposed to noise include necrosis and apoptosis of hippocampal cells; accumulation of amyloid β; tau hyperphosphorylation and peroxidative damage in the hypothalamus and the auditory cortex; and elevated expression of proinflammatory cytokines and microglial activation in the auditory cortex and hippocampus. Human brain scan studies have pointed to the positive relationship between traffic noise exposure and white matter volume in the body of the corpus callosum at the level of the auditory cortex. In conclusion, there is a biological plausibility to the noise-AD relationship, and noise countermeasures may be regarded as the prevention of AD.

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Section: Pathological Concepts Of Noise-ad Relationshipmentioning

confidence: 99%

Noise and Alzheimer's disease

Belojević

2023

Ann Nursing

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“…The cross-functional nature of all of these neuroinflammatory processes across various neurologic diseases may help to explain the high incidence of epileptic seizures in patients with neurological pathologies as diverse as multiple sclerosis [26] or neurodegenerative disease [27]. Figure 1 clarifies the idea that neuroinflammatory mechanisms could be the mediators of epileptogenesis.…”

Section: Introductionmentioning

confidence: 98%

A Systematic Review of the Predictive and Diagnostic Uses of Neuroinflammation Biomarkers for Epileptogenesis

Aguilar-Castillo,

Cabezudo-García,

García-Martín

et al. 2024

IJMS

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A central role for neuroinflammation in epileptogenesis has recently been suggested by several investigations. This systematic review explores the role of inflammatory mediators in epileptogenesis, its association with seizure severity, and its correlation with drug-resistant epilepsy (DRE). The study analysed articles published in JCR journals from 2019 to 2024. The search strategy comprised the MESH, free terms of “Neuroinflammation”, and selective searches for the following single biomarkers that had previously been selected from the relevant literature: “High mobility group box 1/HMGB1”, “Toll-Like-Receptor 4/TLR-4”, “Interleukin-1/IL-1”, “Interleukin-6/IL-6”, “Transforming growth factor beta/TGF-β”, and “Tumour necrosis factor-alpha/TNF-α”. These queries were all combined with the MESH terms “Epileptogenesis” and “Epilepsy”. We found 243 articles related to epileptogenesis and neuroinflammation, with 356 articles from selective searches by biomarker type. After eliminating duplicates, 324 articles were evaluated, with 272 excluded and 55 evaluated by the authors. A total of 21 articles were included in the qualitative evaluation, including 18 case–control studies, 2 case series, and 1 prospective study. As conclusion, this systematic review provides acceptable support for five biomarkers, including TNF-α and some of its soluble receptors (sTNFr2), HMGB1, TLR-4, CCL2 and IL-33. Certain receptors, cytokines, and chemokines are examples of neuroinflammation-related biomarkers that may be crucial for the early diagnosis of refractory epilepsy or may be connected to the control of epileptic seizures. Their value will be better defined by future studies.

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