Abstract:A hallmark of synaptic specializations is their dependence on highly organized complexes of proteins that interact with each other. The loss or modification of key synaptic proteins directly affects the properties of such networks, ultimately impacting synaptic function. SNAP-25 is a component of the SNARE complex, which is central to synaptic vesicle exocytosis, and, by directly interacting with different calcium channels subunits, it negatively modulates neuronal voltage-gated calcium channels, thus regulati… Show more
“…Neurons function depends on the synaptic transmission, in which synapse density proteins play a key role; in AD several studies showed synapses dysfunction and loss to occur before neurons loss, thus attention has been paid to synapse-associated proteins, such as PSD-95 and SNAP-25. PSD-95 is a postsynaptic scaffolding protein that regulates synaptic distribution and activity of glutamate receptors (Tu et al, 2014); SNAP-25 is a component of the SNARE complex, which is central to synaptic vesicle exocytosis, and, by directly interacting with different calcium channels subunits, it negatively modulates neuronal voltage-gated calcium channels, thus regulating intracellular calcium dynamics (Antonucci et al, 2016). SH-SY5Y cells express both synaptic proteins, among others, and reduced levels of these synaptic proteins is expected to alter the cells function.…”
Section: Discussionmentioning
confidence: 99%
“…SH-SY5Y cells express both synaptic proteins, among others, and reduced levels of these synaptic proteins is expected to alter the cells function. Several studies reported that Aβo lead to down-regulation in synaptic markers (Leuba et al, 2008, Feng et al, 2014, Fernandes et al, 2017), and the loss or modification of synaptic proteins directly affects their properties, ultimately impacting synaptic function (Antonucci et al, 2016). …”
Extra-virgin olive oil (EVOO) has several health promoting effects. Evidence have shown that EVOO attenuates the pathology of amyloid-β (Aβ) and improves cognitive function in experimental animal models, suggesting it’s potential to protect and reduce the risk of developing Alzheimer’s disease (AD). Available studies have linked this beneficial effect to oleocanthal, one of the active components in EVOO. The effect of oleocanthal against AD pathology has been linked to its ability to attenuate Aβ and tau aggregation in vitro, and enhance Aβ clearance from the brains of wild type and AD transgenic mice in vivo. However, the ability of oleocanthal to alter the toxic effect of Aβ on brain parenchymal cells is unknown. In the current study, we investigated oleocanthal effect on modulating Aβ oligomers (Aβo) pathological events in neurons and astrocytes. Our findings demonstrated oleocanthal prevented Aβo-induced synaptic proteins, SNAP-25 and PSD-95, down-regulation in neurons, and attenuated Aβo-induced inflammation, glutamine transporter (GLT1) and glucose transporter (GLUT1) down-regulation in astrocytes. Aβo-induced inflammation was characterized by interleukin-6 (IL-6) increase and glial fibrillary acidic protein (GFAP) upregulation that were reduced by oleocanthal. In conclusion, this study provides further evidence to support the protective effect of EVOO-derived phenolic secoiridoid oleocanthal against AD pathology.
“…Neurons function depends on the synaptic transmission, in which synapse density proteins play a key role; in AD several studies showed synapses dysfunction and loss to occur before neurons loss, thus attention has been paid to synapse-associated proteins, such as PSD-95 and SNAP-25. PSD-95 is a postsynaptic scaffolding protein that regulates synaptic distribution and activity of glutamate receptors (Tu et al, 2014); SNAP-25 is a component of the SNARE complex, which is central to synaptic vesicle exocytosis, and, by directly interacting with different calcium channels subunits, it negatively modulates neuronal voltage-gated calcium channels, thus regulating intracellular calcium dynamics (Antonucci et al, 2016). SH-SY5Y cells express both synaptic proteins, among others, and reduced levels of these synaptic proteins is expected to alter the cells function.…”
Section: Discussionmentioning
confidence: 99%
“…SH-SY5Y cells express both synaptic proteins, among others, and reduced levels of these synaptic proteins is expected to alter the cells function. Several studies reported that Aβo lead to down-regulation in synaptic markers (Leuba et al, 2008, Feng et al, 2014, Fernandes et al, 2017), and the loss or modification of synaptic proteins directly affects their properties, ultimately impacting synaptic function (Antonucci et al, 2016). …”
Extra-virgin olive oil (EVOO) has several health promoting effects. Evidence have shown that EVOO attenuates the pathology of amyloid-β (Aβ) and improves cognitive function in experimental animal models, suggesting it’s potential to protect and reduce the risk of developing Alzheimer’s disease (AD). Available studies have linked this beneficial effect to oleocanthal, one of the active components in EVOO. The effect of oleocanthal against AD pathology has been linked to its ability to attenuate Aβ and tau aggregation in vitro, and enhance Aβ clearance from the brains of wild type and AD transgenic mice in vivo. However, the ability of oleocanthal to alter the toxic effect of Aβ on brain parenchymal cells is unknown. In the current study, we investigated oleocanthal effect on modulating Aβ oligomers (Aβo) pathological events in neurons and astrocytes. Our findings demonstrated oleocanthal prevented Aβo-induced synaptic proteins, SNAP-25 and PSD-95, down-regulation in neurons, and attenuated Aβo-induced inflammation, glutamine transporter (GLT1) and glucose transporter (GLUT1) down-regulation in astrocytes. Aβo-induced inflammation was characterized by interleukin-6 (IL-6) increase and glial fibrillary acidic protein (GFAP) upregulation that were reduced by oleocanthal. In conclusion, this study provides further evidence to support the protective effect of EVOO-derived phenolic secoiridoid oleocanthal against AD pathology.
“…SNAP‐25tot did not show any change over time, whereas SNAP‐25aa40 followed the same pattern as GAP‐43, NFL and tau, but it was not significantly altered. This could be due to that SNAP‐25 is expressed in both presynaptic and postsynaptic parts of the neuron, and therefore, the pattern is not as clear in CSF . Nevertheless, considering the function of SNAP‐25aa40 and the trend towards an increase, our data suggest a possible role in recovery after cranial irradiation.…”
Section: Discussionmentioning
confidence: 77%
“…SNAP‐25 and SYT1 are part of or interact with the SNARE complex and play a key role in protein and membrane trafficking, hormone secretion and neurotransmitter release. SNAP‐25 has been shown to be involved in spine maturity . For example, Tomasoni et al .…”
To our knowledge, this is the first time ECM-related proteins have been shown to be affected by cranial radiotherapy in patients with cancer. These findings may help us to get a better understanding of the mechanisms behind side effects following radiotherapy.
“…Its anchoring is due to the palmitoylation of four cysteines located in the center of the protein chain. There are several isoforms of SNAP-25, for example, SNAP-29 and SNAP-23; all are involved in the regulation of exocytosis phenomena [37]. …”
Rapid growth of the overweight population and the number of obese individuals in recent decades suggests that current strategies based on diet, exercise, and pharmacological knowledge are not sufficient to address this epidemic. Obesity is the result of a high caloric intake and energy storage, not counterbalanced by an equally important energy expense. Botulinum toxin type A (BoNT-A) use is rapidly expanding to include treatment of a variety of ophthalmological, gastrointestinal, urological, orthopedic, dermatological, secretory, painful, and cosmetic disorders. Many studies evaluating the effect of BoNT-A in gastric antrum e/o fundus for the treatment of obesity have been published. This treatment modality was based on the observation that gastric injection of BoNT-A in laparatomized rats induced a significant reduction of food intake and body weight. These studies have been published yielding debated results. Differences in the selection of patients, the doses of BoNT-A, the method of administration of the toxin, and the instruments of evaluation of some parameters among these studies may be the cause. In this review, it will study the state-of-the-art use of BoNT-A in obesity basic science models and review the clinical evidence on the therapeutic applications of BoNT-A for obesity.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.