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Łuc, M.;  Woźniak, M.;  Rymaszewska, J. Tumor Necrosis Factor Antagonists in Neuroinflammation for Dementia. Encyclopedia. Available online: https://encyclopedia.pub/entry/39838 (accessed on 17 May 2024).
Łuc M,  Woźniak M,  Rymaszewska J. Tumor Necrosis Factor Antagonists in Neuroinflammation for Dementia. Encyclopedia. Available at: https://encyclopedia.pub/entry/39838. Accessed May 17, 2024.
Łuc, Mateusz, Marta Woźniak, Joanna Rymaszewska. "Tumor Necrosis Factor Antagonists in Neuroinflammation for Dementia" Encyclopedia, https://encyclopedia.pub/entry/39838 (accessed May 17, 2024).
Łuc, M.,  Woźniak, M., & Rymaszewska, J. (2023, January 06). Tumor Necrosis Factor Antagonists in Neuroinflammation for Dementia. In Encyclopedia. https://encyclopedia.pub/entry/39838
Łuc, Mateusz, et al. "Tumor Necrosis Factor Antagonists in Neuroinflammation for Dementia." Encyclopedia. Web. 06 January, 2023.
Tumor Necrosis Factor Antagonists in Neuroinflammation for Dementia
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This entry is adapted from the peer-reviewed paper 10.3390/cells11192959

Prolonged activation of pro-inflammatory responses in Alzheimer’s disease (AD) alters function of glial cells and in turn, further accelerates neuroinflammation. Subsequent synaptic dysfunction and loss of neurons are responsible for clinical symptoms of the disease. Additionally, factors such as insufficient sleep length and subsequent reduction in amyloid clearance via the glymphatic system lead to amyloid accumulation, while simultaneously aggravating systemic inflammatory response. Inflammation in vascular dementia (VaD) contributes to the three-hit hypothesis, along with hypertension and hypoxia. Vasculitis is responsible for restricted blood circulation in microvessels and leads to decreased oxygen supply and regional glial activation favoring neuroinflammation in the central nervous system (CNS). Peripheral immune response and increased cytokine production, including an early surge in TNF and IL-1β concentrations activate glia, leading to aggravation of neuroinflammation and dysfunction of neurons during COVID-19. Lifestyle factors, such as diet, have a large impact on future cognitive outcomes and should be included as a crucial intervention in dementia prevention.

TNF COVID-19 neuroinflammation

1. Tumor Necrosis Factor Triggers Dementia Pathology

Among various cytokines involved in the immune response, tumor necrosis factor (TNF) is considered to play a significant upstream role in dementia pathology on a molecular level. Its pleiotropic effects vary from physiological neuroprotective and repair activities to pathological neuronal loss occurring in neurodegenerative and autoimmune conditions which are dependent on TNF form and activated receptor [1]. TNF receptor type 1 (TNFR1) is commonly expressed and can be bound by both transmembrane and soluble TNF forms, while TNF receptor type 2 (TNFR2), expressed by myeloid and endothelial cells but also by CNS-residing glia and neurons, is mainly bound by transmembrane TNF [2]. Protective versus deleterious outcomes of receptor activation depend on various factors including TNF concentration, activation of other signaling pathways or cell susceptibility resulting from cell type and age-related priming [3][4]. TNF signaling activates intracellular pathways with transcription factors such as NFκB (nuclear factor kappa-light-chain-enhancer of activated B cells) leading to pro-inflammatory cytokine production and, in conditions of prolonged signaling, aggravation of inflammation [5][6].
Exposure to TNF in an in vitro AD model has been shown to result in aggregation of extracellular proteins which are considered characteristic traits of AD and LBD pathology [7]. Interestingly, exposure to TNF does not need to be sustained in order to maintain increased secretion and aggregation of amyloid-β or α-synuclein in such models. This mechanism may demonstrate profound effects of TNF signaling on pro-inflammatory activation and cytokine production of astrocytes and microglia, leading to prolonged neuroinflammation [8]. This phenomenon has been reflected in a cohort study by Lindbergh et al., in which TNF plasma concentration of participants were assessed annually. Increased systemic TNF resulted in reduction in grey matter volumes in further assessments in a curvilinear correlation, with initially-increased TNF correlating with following loss of volume [9]. Additionally, within-person increases in TNF correlated with lower scores obtained in neuropsychological evaluation with the use of Mini Mental State Examination.

2. Methods for Reduction of Pro-Inflammatory Activation

Since TNF signaling exerts a triggering effect in the development of cognitive decline [7][9], the question arises, whether interventions focused on reduction in TNF concentrations or inhibition of its signaling pathway may play a role in dementia prevention or treatment. There are several methods of reducing an inflammatory state in the human organism, including dietary and pharmacological interventions.
Diet has been implicated in pathology of numerous neurodegenerative diseases, including dementia. A well-balanced diet provides all nutritional ingredients necessary for maintaining healthy and functional neurons [10]. On the other hand, it is believed that diet largely impacts inflammatory activation and immune response, which in turn influences regional inflammatory response in the brain. Various studies, including large cohorts, have associated inflammatory dietary patterns with faster cognitive decline and subsequent cognitive impairment [11][12][13]. The correlation between inflammatory diet and cognition is especially apparent in regard to several cognitive functions, such as episodic memory, semantic-based memory, executive functions and working memory [14].
The Western diet which comprises highly-processed food rich in fructose and saturated fat is known to increase TNF concentration in animal models [15]. Mice immunized against Klebsiella pneumoniae were shown to have lower levels of inflammasome-related inflammation, providing yet another link between gut microbiota and inflammation. This phenomenon was mediated by the presence of apolipoprotein E and was not observed in ApoE −/− animals [15]. Although individually tailored diets are not yet within reach and require further exploration, some conclusions regarding the influence of particular diets on neurodegenerative processes can be made based on existing studies [16]. For example, use of Dietary Inflammatory index (DII), which takes into account individual’s dietary composition and characteristics, allows researchers to indicate the general influence of one’s diet on systemic cytokine levels and inflammatory activation [17]. Higher scores of DII were shown to strongly correlate with worse cognitive performance [18]. It stands to reason, that the influence of environmental factors such as diet in preserving cognition cannot be underestimated. On the other hand, it seems that the inflammatory potential of the consumed food may be related not only to the specific products but also to the gut microbiota composition resulting from the daily diet. A summary of findings associated with specific diets can be found in Table 1 [19][20][21][22][23][24][25][26][27][28].
Table 1. Summary of findings associated with diet and inflammation.
Study (Type) Outcomes Diet/Intervention Group Key Findings
Ostan et al., 2015 [19]
(cohort study)		 Inflammatory and metabolic parameters RISTOMED diet (personalized and balanced)
+/− nutraceutics		 125 participants RISTOMED diet alone or with each nutraceutical supplementation significantly decreased erythrocyte sedimentation rate
Kim et al., 2022 [20]
(non-randomized intervention study)		 Inflammatory parameters
Insulin sensitivity		 Short-term ketogenic diet (3 days) 15 participants Short-term Ketogenic diet resulted in lower IL-1β and TNF secretion;
Improved insulin sensitivity
Al-Abauidy et al., 2021 [21]
(randomized clinical trial)		 Oxidative stress and inflammatory parameters Mediterranean diet (12 weeks) 19 participants Mediterranean diet reduced IL-6 levels by 49% and levels of oxidative stress marker, 8-OHdG, by 32.4%
Georgoulis et al., 2021 [22]
(randomized clinical trial)		 Oxidative stress and inflammatory parameters Mediterranean diet (6 months) 187 patients with obstructive sleep apnea Mediterranean diet reduced hs-CRP levels in patients
Casas et al., 2017 [25]
(randomized clinical trial)		 Cytokine levels Mediterranean diet +/− extra virgin olive oil (5 years) 66 participants Mediterranean diet reduced IL-6, IL-8, MCP-1, and MIP-1β levels. Addition of extra virgin olive oil reduced IL-1β, IL-5, IL-7, IL-12p70, IL-18, TNF-α, IFN-γ, GCSF, GMCSF, and ENA78
Omorogieva et al., 2021 [23]
(meta-analysis)		 Lipid profiles, LPS, BMI, inflammatory markers Diet rich in fiber 10 studies included in meta-analysis Dietary fiber reduces total cholesterol, BMI and CRP, but no significant changes were observed for IL-6 and TNF
Shivappa et al., 2016 [24]
(cross-sectional study)		 Inflammatory markers - 532 adolescents Higher dietary inflammatory index scores were associated with increased levels of various inflammatory markers: TNF-α, IL-1, 2, IFN-γ and VCAM
Mazzoli et al., 2020 [26]
(animal study)		 Inflammatory markers, insulin sensitivity, BDNF Western diet (4 weeks) 16 rats Western diet increased TNF levels in white adipose tissue and hippocampus of rats; brain BDNF and synaptotagmin I were decreased, while PSD-95 was increased.
Jena et al., 2020 [27]
(animal study)		 Interleukin-17, PD-95, BDNF High sugar and high fat diet (FPC diet) for 3 months, and 5 months +/− inulin supplementation 12 mice FPC diet elevated RORγ and IL-17A signaling. Accompanied by microglia activation and reduced hippocampal long-term potentiation, FPC diet intake also reduced postsynaptic density-95 and brain derived neurotrophic factor.
Godfrey et al., 2020 [28]
(animal study)		 CRP levels, CSF dopamine concentrations
Functional connectivity		 12 months of obesogenic diet 34 female rhesus monkeys CSF dopamine concentrations decreased, and CRP concentrations increased. Resting-state magnetic resonance neuroimaging showed that higher CRP concentrations were associated with decreased functional connectivity.
Non-steroidal anti-inflammatory drugs (NSAIDs), the most commonly used anti-inflammatory drugs, were considered as potential dementia preventive agents in numerous studies. Some animal and human cohort studies suggested a beneficial influence of a daily intake of specific NSAIDs in preventing development or progression of most common types of dementia via reducing distinct dementia pathology [29][30][31]. However, large randomized clinical-trials or meta-analyses did not provide strong evidence supporting their recommended use, with a special regard to the dangerous side effects of their daily intake, such as potential gastrointestinal bleeding [32][33][34][35][36][37][38][39].
TNF antagonists offer yet another interesting approach to reducing inflammatory activation in humans. These agents are commonly used in autoimmune diseases, such as rheumatoid arthritis, psoriasis or inflammatory bowel diseases [40]. Their effects in controlling excessive immune response are mediated by binding TNF but the exact mechanisms and affinity to soluble and transmembrane TNF vary, hence their clinical use can also differ [4][41][42]. Moreover, some other mechanisms of action have been described, such as lymphotoxin-α blocking by etanercept. Additionally, infliximab has been proven to reduce expression of GM-CSF (granulocyte-macrophage colony stimulating factor) [43][44], while infliximab and adalimumab are able to induce production of immunosuppressive IL-10 by macrophages in vitro [45]. Psoriasis patients treated with etanercept had decreased expression of IL-1 and IL-8 genes which correlated with reduction in total pro-inflammatory immune response [46]. Importantly, although molecular weight and properties do not allow for free entry of TNF antagonists into the CNS, evidence indicates that these drugs may have protective influence against brain aging.
It seems that both BBB-nonpenetrating and modified, BBB-penetrating, etanercept reduce tauopathy, microgliosis and therefore, neuronal loss in a mouse model of AD. Additionally, they increase PSD95 protein levels indicating synaptic health. This phenomenon may be related to the peripheral effects of the drug and underlines the importance of tackling chronic inflammatory activation in order to maintain physiological neuronal function [47]. Similar observations had been made previously, in a study by Chang et al. [48]. Administration of BBB-penetrating TNF-inhibitor, cTfRMAb-TNFR, resulted in a significant decrease in neuroinflammatory markers, amyloid burden and BBB disruption in an AD mouse model. These results were comparable to those obtained with the use of etanercept in regard to amyloid burden and BBB integrity but not for neuroinflammation portrayed with ICAM-1 concentration. The cognitive performance of tested mice was highest in a group treated with cTfRMAb-TNFR highlighting the crucial role of neuroinflammation in cognitive decline [48]. Use of BBB-penetrating agents remains especially interesting in regard to FTD pathology, in which cytokine production seems to take place mainly in the brain [49].
An experiment conducted in an animal model of metabolic syndrome proved that intraperitoneal administration of infliximab improved lipid profiles in rats—i.e., decreased triglycerides and increased HDL. Additionally, the study group had lower adiponectin concentrations compared to the control, impacting low-grade inflammation. Noteworthy, not all metabolic aspects were normalized and cognitive tests were not included in the study protocol [50]. It may be hypothesized that an up-stream role of TNF in obesity-induced pathology, limits the potential protective effects of TNF inhibition in conditions of already present metabolic syndrome. On the other hand, intracerebroventricular administration of infliximab in a transgenic mouse model of AD resulted in a significant decrease in brain TNF levels, reduction in amyloid burden and tau pathology [51]. Another study conducted in a rat model of VaD, revealed a therapeutic effect of adalimumab administration in treating cognitive deficits resulting from cerebral hypoperfusion. This finding was associated with a reduction in neuronal loss and of microglial activation mediated by NFκB suppression [52].
A systematic literature review of TNF antagonist effects on AD revealed beneficial influence of TNF inhibition on cognition [5]. Most commonly studied agents, etanercept, infliximab and adalimumab, used in rheumatoid arthritis coincided with up to 60–70% reduction in AD incidence in large epidemiological analyzes of rheumatoid arthritis patients, whereas other methods of treatment did not affect AD incidence [53]. Similar results were obtained in patients with psoriasis who were treated with etanercept, infliximab or adalimumab [54]. Rheumatoid arthritis and psoriasis, among other autoimmune diseases, are known risk factors of AD due to the occurrence of persistent inflammatory activation which may constitute a confounding factor for generalized conclusions [55][56][57]. However, these observations warrant further research in other populations in order to establish a protective role of TNF inhibition on development and progression of various types of dementia. Updates on current clinical trials can be found in Table 2.
Table 2. Updates on clinical trials with the use of agents which potentially reduce neuroinflammation.
Anti-Inflammatory Agent Clinicaltrial.gov Indentifier Clinical Trial Phase Results
Etanercept
(TNF antagonist)		 NCT01068353, NCT01716637, NCT00203359, NCT00203320 1–2 Etanercept was well tolerated and showed some trends toward cognitive, functional, and behavioral benefits
XPro1595/DN-TNF
(TNF antagonist)		 NCT03943264, NCT05321498, NCT05522387, NCT05318976 1,2 In phase 1 XPro1595 reduced white matter free water and increased the axonal integrity in adults with mild to moderate Alzheimer’s disease with signs of inflammation.
Phase 2 trials are currently active
Dapagliflozin
(selective sodium-glucose cotransporter 2 inhibitor)		 NCT03801642 1/2 Trial ongoing;
Alongside beneficial metabolic effects a potential anti-inflammatory effect via reduction in oxidative stress
ALZT-OP1/cromolyn + ibuprofen
(mast cell stabilizer + NSAID)		 NCT04570644, NCT02547818 1/2, 3 The combination of cromolyn and ibuprofen was safe and well tolerated. The concentrations of cromolyn and ibuprofen observed in the CSF are considered sufficient to titrate the estimated daily amyloid production and the associated inflammatory response in patients with AD.
Phase 3 results are to be published.
Senicapoc
(KCa3.1 blocker)		 NCT04804241 2 Phase 2 trial is currently active.
Previous animal studies show reduced neuroinflammation, decreased cerebral amyloid load, and enhanced hippocampal neuronal plasticity [58].

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Subjects: Geriatrics & Gerontology
Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register :
Mateusz Łuc
,
Marta Woźniak
,
Joanna Rymaszewska
View Times: 294
Entry Collection: Neurodegeneration
Revisions: 3 times (View History)
Update Date: 09 Jan 2023
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