Neuronutraceuticals Modulate Lipopolysaccharide- or Amyloid-β 1-42 Peptide-Induced Transglutaminase 2 Overexpression as a Marker of Neuroinflammation in Mouse Microglial Cells

Gatta, Nicola Gaetano; Parente, Andrea; Guida, Francesca; Maione, Sabatino; Gentile, Vittorio

doi:10.3390/app11125718

Cited by 4 publications

(7 citation statements)

References 32 publications

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“…Also, PEA was found to exert protective properties in wild-type mouse cell cultures but not in AD mouse neuronal cultured cells overexpressing Aβ, suggesting its effectiveness in early AD or when Aβ is accumulating and initiating damage in the central nervous system ( 35 ). Similar findings were found among AD models where in vitro PEA application reduced neuroinflammation ( 52 ) and astrogliosis ( 38 , 45 ), supporting neuronal viability and survival ( 38 , 45 ), and also improving enteric inflammation ( 50 ).…”

Section: Resultssupporting

confidence: 79%

“…To confirm the results obtained with the in vitro models, some studies made the same PEA treatment ex vivo (Tables 1B, 2B) with organotypic cultures challenged with Aβ (22, 32, 33) or lipopolysaccharide (LPS) (52). Converging evidence suggests that PEA may enhance neuroprotection against the neurodegenerative processes associated with Aβ deposition, including astrocyte activation (32, 33) and neuroinflammation (32, 33, 52).…”

Section: Ex Vivo Pea Exposure In In Aβ Exposed Animal Cells and Ad An...mentioning

confidence: 78%

“…In total, 11 studies evaluated the effect of in vitro PEA exposure on several neurobiological mechanisms underlying NCDs ( Tables 1B , 2B ), using both Aβ exposed animal cells ( 25 , 29 , 30 , 32 , 33 , 35 , 37 ) and AD animal model cells ( 38 , 45 , 50 , 52 ). PEA application was reported to reduce Aβ-induced neuroinflammation and astrocyte activation ( 25 , 29 , 30 , 32 , 33 , 37 ) as well as angiogenesis ( 25 ), exerting a protective effect on neuronal cells ( 32 , 33 , 37 ).…”

Section: Resultsmentioning

confidence: 99%

“…Converging evidence suggests that PEA may enhance neuroprotection against the neurodegenerative processes associated with Aβ deposition, including astrocyte activation ( 32 , 33 ) and neuroinflammation ( 32 , 33 , 52 ). Also, PEA exposure showed specific effects in reducing inducible nitric oxide synthase ( 22 ), glial fibrillary acidic protein expression ( 22 ), and apoptosis ( 22 , 52 ) as well as restoring neuronal nitric oxide synthase ( 22 ) and brain derived neurotrophic factor (BDNF) ( 22 ).…”

Section: Resultsmentioning

confidence: 99%

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Therapeutic effect of palmitoylethanolamide in cognitive decline: A systematic review and preliminary meta-analysis of preclinical and clinical evidence

et al. 2022

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Cognitive decline is believed to be associated with neurodegenerative processes involving excitotoxicity, oxidative damage, inflammation, and microvascular and blood-brain barrier dysfunction. Interestingly, research evidence suggests upregulated synthesis of lipid signaling molecules as an endogenous attempt to contrast such neurodegeneration-related pathophysiological mechanisms, restore homeostatic balance, and prevent further damage. Among these naturally occurring molecules, palmitoylethanolamide (PEA) has been independently associated with neuroprotective and anti-inflammatory properties, raising interest into the possibility that its supplementation might represent a novel therapeutic approach in supporting the body-own regulation of many pathophysiological processes potentially contributing to neurocognitive disorders. Here, we systematically reviewed all human and animal studies examining PEA and its biobehavioral correlates in neurocognitive disorders, finding 33 eligible outputs. Studies conducted in animal models of neurodegeneration indicate that PEA improves neurobehavioral functions, including memory and learning, by reducing oxidative stress and pro-inflammatory and astrocyte marker expression as well as rebalancing glutamatergic transmission. PEA was found to promote neurogenesis, especially in the hippocampus, neuronal viability and survival, and microtubule-associated protein 2 and brain-derived neurotrophic factor expression, while inhibiting mast cell infiltration/degranulation and astrocyte activation. It also demonstrated to mitigate β-amyloid-induced astrogliosis, by modulating lipid peroxidation, protein nytrosylation, inducible nitric oxide synthase induction, reactive oxygen species production, caspase3 activation, amyloidogenesis, and tau protein hyperphosphorylation. Such effects were related to PEA ability to indirectly activate cannabinoid receptors and modulate proliferator-activated receptor-α (PPAR-α) activity. Importantly, preclinical evidence suggests that PEA may act as a disease-modifying-drug in the early stage of a neurocognitive disorder, while its protective effect in the frank disorder may be less relevant. Limited human research suggests that PEA supplementation reduces fatigue and cognitive impairment, the latter being also meta-analytically confirmed in 3 eligible studies. PEA improved global executive function, working memory, language deficits, daily living activities, possibly by modulating cortical oscillatory activity and GABAergic transmission. There is currently no established cure for neurocognitive disorders but only treatments to temporarily reduce symptom severity. In the search for compounds able to protect against the pathophysiological mechanisms leading to neurocognitive disorders, PEA may represent a valid therapeutic option to prevent neurodegeneration and support endogenous repair processes against disease progression.

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Section: Resultssupporting

confidence: 79%

Section: Ex Vivo Pea Exposure In In Aβ Exposed Animal Cells and Ad An...mentioning

confidence: 78%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

See 2 more Smart Citations

Therapeutic effect of palmitoylethanolamide in cognitive decline: A systematic review and preliminary meta-analysis of preclinical and clinical evidence

et al. 2022

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“…Several findings demonstrated that CUR shows strong neuro-protective effects improving cognitive function; promoting axonal regeneration [ 23 , 24 , 25 , 26 , 27 , 28 ]; reducing apoptotic proteins; upregulating the anti-apoptotic protein Bcl-2; and also stimulating neurogenesis and neuroplasticity. In addition, recent data demonstrated that CUR is able to downregulate TG2 overexpression in mouse microglial cells (exposed to lipopolysaccharide or Aβ 1–42 full peptide), thus suggesting its possible use for neuroprotection in neuroinflammatory pathologies, including AD [ 29 ]. In vitro and in vivo studies on AD models also demonstrated that CUR was able to inhibit the formation of Aβ oligomers [ 30 , 31 ].…”

Section: Introductionmentioning

confidence: 99%

Effect of Unloaded and Curcumin-Loaded Solid Lipid Nanoparticles on Tissue Transglutaminase Isoforms Expression Levels in an Experimental Model of Alzheimer’s Disease

et al. 2022

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Alzheimer’s disease (AD) is a neurodegenerative disease representing the most prevalent cause of dementia. It is also related to the aberrant amyloid-beta (Aβ) protein deposition in the brain. Since oxidative stress is involved in AD, there is a possible role of antioxidants present in the effected person’s diet. Thus, we assessed the effect of the systemic administration of solid lipid nanoparticles (SLNs) to facilitate curcumin (CUR) delivery on TG2 isoform expression levels in Wild Type (WT) and in TgCRND8 (Tg) mice. An experimental model of AD, which expresses two mutated human amyloid precursor protein (APP) genes, was used. Behavioral studies were also performed to evaluate the improvement of cognitive performance and memory function induced by all treatments. The expression levels of Bcl-2, Cyclin-D1, and caspase-3 cleavage were evaluated as well. In this research, for the first time, we demonstrated that the systemic administration of SLNs-CUR, both in WT and in Tg mice, allows one to differently modulate TG2 isoforms, which act either on apoptotic pathway activation or on the ability of the protein to repair cellular damage in the brains of Tg mice. In this study, we also suggest that SLNs-CUR could be an innovative tool for the treatment of AD.

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2-pentadecyl-2-oxazoline prevents cognitive and social behaviour impairments in the Amyloid β-induced Alzheimer-like mice model: Bring the α2 adrenergic receptor back into play

Infantino¹,

Boccella²,

Scuteri³

et al. 2022

Biomedicine & Pharmacotherapy

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Neuronutraceuticals Modulate Lipopolysaccharide- or Amyloid-β 1-42 Peptide-Induced Transglutaminase 2 Overexpression as a Marker of Neuroinflammation in Mouse Microglial Cells

Cited by 4 publications

References 32 publications

Therapeutic effect of palmitoylethanolamide in cognitive decline: A systematic review and preliminary meta-analysis of preclinical and clinical evidence

Therapeutic effect of palmitoylethanolamide in cognitive decline: A systematic review and preliminary meta-analysis of preclinical and clinical evidence

Effect of Unloaded and Curcumin-Loaded Solid Lipid Nanoparticles on Tissue Transglutaminase Isoforms Expression Levels in an Experimental Model of Alzheimer’s Disease

2-pentadecyl-2-oxazoline prevents cognitive and social behaviour impairments in the Amyloid β-induced Alzheimer-like mice model: Bring the α2 adrenergic receptor back into play

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