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Nanoemulsion for Brain Targeting
Published in Raj K. Keservani, Anil K. Sharma, Rajesh K. Kesharwani, Nanocarriers for Brain Targeting, 2019
Khushwinder Kaur, Shivani Uppal
Neuroinflammation is a hallmark of acute and chronic neurodegenerative disorders. The main aim of the study conducted by Yadav et al. was to evaluate the therapeutic efficacy of intranasal cationic nanoemulsion encapsulating an anti-TNFa siRNA, for potential anti-inflammatory therapy. TNFa siRNA nanoemulsions were prepared and characterized for particle size, surface charge, morphology, and stability and encapsulation efficiency. Qualitative and quantitative intracellular uptake studies by confocal imaging and flow cytometry, respectively, showed higher uptake compared to Lipofectamine® transfected siRNA. Nanoemulsion significantly lowered TNFa levels in LPS-stimulated cells. Upon intranasal delivery of cationic nanoemulsions, almost fivefold higher uptake was observed in the rat brain compared to nonencapsulated siRNA. More importantly, intranasal delivery of TNFa siRNA nanoemulsions in vivo markedly reduced the unregulated levels of TNFa in an LPS-induced model of neuro-inflammation. These results indicated that intranasal delivery of cationic nanoemulsions encapsulating TNFa siRNA offered an efficient means of gene knockdown and this approach has significant potential in the prevention of neuroinflammation (Yadav et al., 2016).
Alzheimer’s Disease: Potential of Nanotailored Nutraceuticals
Published in Bhupinder Singh, Minna Hakkarainen, Kamalinder K. Singh, NanoNutraceuticals, 2019
Vandita Kakkar, Komal Saini, Suneera Adlakha, Indu Pal Kaur
The inflammatory mechanisms involved in the cascade of neuroinflammation are related to the involvement of brain cells (e.g., microglia and astrocytes), the classic and alternate pathways of the complement system, the pentraxin acute-phase proteins, neuronal-type nicotinic acetylcholine receptors (AChRs), peroxisomal proliferators-activated receptors (PPARs), and cytokines as well as chemokines (Figure 7.4). This signifies the setting in of the neuroinflammation to be an extremely interactive process, wherein the first to counteract the neuronal injuries are the microglial cells, which are the brain macrophages (Dheen et al., 2007). In AD, a cleavage of the APP and the aggregation of Aβ peptides (Aβ1-42 and Aβ1-40) trigger the activation of microglials and astrocytes, following activation of transcription factors (i.e., nuclear factor-kappa B [NF-kB] and activator protein [AP]-1), persuading the prolongation of ROS and several other proinflammatory mediators (Dheen et al., 2007). The liberation of these pro-inflammatory cytokines and ROS further cause the neuronal destruction or neurotoxicity, resulting in apoptosis as well as necrosis. These pro-inflammatory mediators from the microglials and astrocytes can also stimulate each other to strengthen the signs of inflammatory signals to the neurons (Pan et al., 2010).
Clinical Effects of Pollution
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 5, 2017
William J. Rea, Kalpana D. Patel
Recently, we learned the pain that initially arises from a peripheral nervous system injury may become imprinted or “embedded” in the CNS, activate microglial cells (Figure 2.12), and produce neuroinflammation. This phenomenon of “central sensitization” and the resulting state is centralized pain (CP).96–98 This pain is seen in many chemically sensitive patients and may result in blockage of areas in the brain of glia cells and lymphatic waste removal. Phantom limb pain is the classic example. Other examples include neuropathies, including complex regional pain syndrome and diabetic neuropathies. Disorders that originate in the CNS, such as trauma, stroke, infections, and arachnoiditis, also cause significant neuroinflammation (Figure 2.14).
Inflammatory and apoptotic signalling pathways and concussion severity: a genetic association study
Published in Journal of Sports Sciences, 2018
Sarah Mc Fie, Shameemah Abrahams, Jon Patricios, Jason Suter, Michael Posthumus, Alison V. September
Although neuroinflammation is necessary to promote healing in the central nervous system, a prolonged or over-active response can have detrimental effects on the health of nervous tissue (Lenzlinger, Morganti-Kossmann, Laurer, & McIntosh, 2001; Morganti-Kossmann, Rancan, Stahel, & Kossmann, 2002). For example, increased blood brain barrier disruption resulted in prolonged inflammatory stimulation, oedema, and cell death (Schlosberg, Benifla, Kaufer, & Friedman, 2010), while increased neuronal apoptosis caused disruption of white matter networks and neurological difficulties (Kraus et al., 2007). Furthermore, activated microglia and astroglia release several neurotoxic chemicals, including nitric oxide, which can be damaging to the health of surrounding neurons (Brown & Neher, 2010).
Acute exercise increases BDNF serum levels in patients with Parkinson’s disease regardless of depression or fatigue
Published in European Journal of Sport Science, 2022
Lílian Viana dos Santos Azevedo, Jéssica Ramos Pereira, Renata Maria Silva Santos, Natalia Pessoa Rocha, Antônio Lúcio Teixeira, Paulo Pereira Christo, Victor Rodrigues Santos, Paula Luciana Scalzo
Moreover, neuroinflammation has been associated with non-motor PD symptoms, such as depression and fatigue, and an association between inflammation and neural plasticity is suggested (Golia et al., 2019). Interestingly, excessive levels of inflammatory mediators have been associated with a decrease in plasticity-promoting factors, including BDNF (Golia et al., 2019). Individuals with PD and depression present lower BDNF serum levels when compared to control subjects (Rahmani et al., 2019), while individuals with PD and fatigue present higher interleukin-6 (IL-6) serum levels (Pereira et al., 2016).
Melatonin attenuates expression of cyclooxygenase-2 (COX-2) in activated microglia induced by lipopolysaccharide (LPS)
Published in Journal of Toxicology and Environmental Health, Part A, 2019
Chunyan Yao, Xiaoling Liu, Zhengyu Zhou, Ying Xiang, Shuai Yuan, Weijia Xie, Meiyu Zhou, Zeyao Hu, Yafei Li, Ailing Ji, Tongjian Cai
Neuroinflammation is a consequential response observed in neurodegenerative diseases, including Parkinson’s, Alzheimer’s, and Huntington’s diseases (Foucault-Fruchard and Antier 2017; Huo et al. 2016; Jia et al. 2018; Li and Le 2013; Valdiglesias et al. 2017). Associated with the hyperactivity of immune cells within the central nervous system (CNS), neuroinflammation has emerged as a consequence observed in neurodegenerative disorders (Singh et al. 2017).