A combination of lycopene and human amniotic epithelial cells can ameliorate cognitive deficits and suppress neuroinflammatory signaling by choroid plexus in Alzheimer's disease rat

Xu, Zhengguo; Liu, Chao; Wang, Rui; Gao, Xi-Ren; Hao, Chao; Liu, Chongbin

doi:10.1016/j.jnutbio.2020.108558

Cited by 24 publications

(23 citation statements)

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“…We here document inflammatory changes and perturbed protein and lipid metabolism in the ChP harvested from patients with AD compared to healthy controls. These findings are in agreement with the reported upregulation of inflammatory networks in the ChP in patients with AD (Kant et al, 2018;Steeland et al, 2018) and in animal models of AD (Brkic et al, 2015;Mesquita et al, 2015;Xu et al, 2020). Coupled to the observed deleterious effects of the inflammatory molecules on the ChP in culture (Schwerk et al, 2010), these reports suggest that inflammatory changes compromise the structural integrity of the ChP (Brkic et al, 2015;Gonzalez-Marrero et al, 2015;Kant et al, 2018;Pearson et al, 2020;Serot et al, 2000) and contribute to impaired CSF production in AD (Silverberg et al, 2001).…”

Section: Discussionsupporting

confidence: 89%

“…Recent work reveals that the structure and function of the ChP change dramatically during aging (Baruch et al, 2014;Serot et al, 2000;Zhu et al, 2018) and in Alzheimer's disease (AD), a major age-related disorder (Kant et al, 2018;Serot et al, 2000). These changes are further corroborated in animal models of AD (Brkic et al, 2015;Gonzalez-Marrero et al, 2015), which also show elevated cytokine levels in the ChP (Balusu et al, 2016a;Baruch et al, 2015;Brkic et al, 2015;Steeland et al, 2018) and reversal of select AD phenotypes by attenuating the inflammatory response of the ChP (Baruch et al, 2015;Xu et al, 2020). In agreement with this work, besides impaired production and composition (Gate et al, 2020;Silverberg et al, 2001;Taipa et al, 2019), the CSF demonstrates inflammatory changes involving increased levels of glial markers (Llorens et al, 2017) and cytokines in both aging (Hu et al, 2019;Racine et al, 2019;Sala-Llonch et al, 2017) and AD (Brosseron et al, 2020;Craig-Schapiro et al, 2010;Hu et al, 2019;Rauchmann et al, 2020;Rauchmann et al, 2019;Taipa et al, 2019).…”

Section: Introductionmentioning

confidence: 99%

“…Consistent with these findings, animal models of major age-related disorders such as Alzheimer's disease (AD), also exhibit inflammatory changes in the ChP 15 . In these models, the ChP shows increased levels of cytokines such as tumour necrosis factor alpha (TNFa) [16][17][18] , perturbed secretion of proteins such as transthyretin (TTR) 19 , disruption of the BCSFB 18,19 and reversal of select AD phenotypes by attenuating the ChP inflammatory response 16,20 . These findings, together with reported interaction between amyloid peptides and the ChP volume 21 , morphological changes of the BCSFB 22,23 and impaired production and inflammatory abnormalities of the CSF 4,5,24 in AD patients, all suggest a relationship between aging, ChP dysfunction and AD.…”

mentioning

confidence: 99%

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Pathogenesis of Alzheimer’s disease: Involvement of the Choroid Plexus

Čarná

Onyango

Katina

et al. 2021

Preprint

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Alzheimer's disease is a neurodegenerative disorder characterized clinically by cognitive decline and pathologically by amyloid deposition and neurofibrillary changes. These neuropathological hallmarks are accompanied by reactive events including microglial activation and astrogliosis. The inflammatory response in Alzheimer's disease brains is distinguished by a pro-inflammatory signature involving amyloid peptides, inflammasome signalling and disrupted blood brain barrier. Inflammatory changes are observed also in the cerebrospinal fluid in Alzheimer's disease. It remains unknown, however, whether the choroid plexus which produces cerebrospinal fluid and guards the brain from peripheral inflammatory insults, contributes to the inflammation and pathogenesis of Alzheimer's disease. Here we show that the choroid plexus in Alzheimer's disease exhibits a pro-inflammaotory signature with aberrant protein accumulation, which contribute to the age-dependent inflammatory changes observed in the cerebrospinal fluid. Magnetic resonance imaging reveals that the choroid plexus in patients with Alzheimer's disease displays pathological signal and increased volume, which inversely correlates with cognitive decline. Our findings suggest that the choroid plexus, being unable to efficiently resolve inflammatory insults over the lifetime, eventually ignites and drives the aberrant inflammatory response observed in Alzheimer's disease. These findings advance our understanding of the pathogenesis and open new vistas in the diagnostics and therapeutics of Alzheimer's disease.

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Section: Discussionsupporting

confidence: 89%

Section: Introductionmentioning

confidence: 99%

mentioning

confidence: 99%

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Pathogenesis of Alzheimer’s disease: Involvement of the Choroid Plexus

Čarná

Onyango

Katina

et al. 2021

Preprint

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“…Nuclear factor-k-gene binding (NF-κB) is a key regulator of inflammation-related gene expression in human cells, and LPS can stimulate NF-κB expression by binding to Toll-like receptor 4 (TLR4). ( Tiruppathi et al, 2008 ; Verstrepen et al, 2008 ; Xu et al, 2021 ). Hu et al found that LPS can destroy BBB by reducing the level of occludin through TLR4/NF-κB pathway ( Hu et al, 2017 ).…”

Section: Direct Effectsmentioning

confidence: 99%

“…NF-κB, as a proinflammatory cell transcription factor that exists in almost all cells, was found to participate in the BBB disruption by LPS ( Xu et al, 2021 ). Nod-like receptor protein 3 (NLRP3) plays an important role in the inflammation cascade by amplifying the inflammation response ( Islam et al, 2020 ).…”

Section: Bbb and Saementioning

confidence: 99%

Blood-Brain Barrier Disruption by Lipopolysaccharide and Sepsis-Associated Encephalopathy

Peng

Luo

et al. 2021

Front. Cell. Infect. Microbiol.

113

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As a complex multicellular structure of the vascular system at the central nervous system (CNS), the blood-brain barrier (BBB) separates the CNS from the system circulation and regulates the influx and efflux of substances to maintain the steady-state environment of the CNS. Lipopolysaccharide (LPS), the cell wall component of Gram-negative bacteria, can damage the barrier function of BBB and further promote the occurrence and development of sepsis-associated encephalopathy (SAE). Here, we conduct a literature review of the direct and indirect damage mechanisms of LPS to BBB and the relationship between these processes and SAE. We believe that after LPS destroys BBB, a large number of inflammatory factors and neurotoxins will enter and damage the brain tissue, which will activate brain immune cells to mediate inflammatory response and in turn further destroys BBB. This vicious circle will ultimately lead to the progression of SAE. Finally, we present a succinct overview of the treatment of SAE by restoring the BBB barrier function and summarize novel opportunities in controlling the progression of SAE by targeting the BBB.

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Pathogenesis of Alzheimer's disease: Involvement of the choroid plexus

Čarná

Onyango

Katina

et al. 2023

Alzheimer's & Dementia

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The choroid plexus (ChP) produces and is bathed in the cerebrospinal fluid (CSF), which in aging and Alzheimer's disease (AD) shows extensive proteomic alterations including evidence of inflammation. Considering inflammation hampers functions of the involved tissues, the CSF abnormalities reported in these conditions are suggestive of ChP injury. Indeed, several studies document ChP damage in aging and AD, which nevertheless remains to be systematically characterized. We here report that the changes elicited in the CSF by AD are consistent with a perturbed aging process and accompanied by aberrant accumulation of inflammatory signals and metabolically active proteins in the ChP. Magnetic resonance imaging (MRI) imaging shows that these molecular aberrancies correspond to significant remodeling of ChP in AD, which correlates with aging and cognitive decline. Collectively, our preliminary post‐mortem and in vivo findings reveal a repertoire of ChP pathologies indicative of its dysfunction and involvement in the pathogenesis of AD.Highlights Cerebrospinal fluid changes associated with aging are perturbed in Alzheimer's disease Paradoxically, in Alzheimer's disease, the choroid plexus exhibits increased cytokine levels without evidence of inflammatory activation or infiltrates In Alzheimer's disease, increased choroid plexus volumes correlate with age and cognitive performance

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A combination of lycopene and human amniotic epithelial cells can ameliorate cognitive deficits and suppress neuroinflammatory signaling by choroid plexus in Alzheimer's disease rat

Cited by 24 publications

References 58 publications

Pathogenesis of Alzheimer’s disease: Involvement of the Choroid Plexus

Pathogenesis of Alzheimer’s disease: Involvement of the Choroid Plexus

Blood-Brain Barrier Disruption by Lipopolysaccharide and Sepsis-Associated Encephalopathy

Pathogenesis of Alzheimer's disease: Involvement of the choroid plexus

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