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347 results on '"Ramassamy,Charles"'

1. Infection, Neuroinflammation and Interventions for Healthy Brain and Longevity

Author

Fülöp, Tamàs, Ramassamy, Charles, Lacombe, Guy, Frost, Eric H., Cohen, Alan A., Rodrigues, Serafim, Desroches, Mathieu, Hirokawa, Katsuiku, Laurent, Benoit, Witkowski, Jacek M., Rattan, Suresh I.S., Editor-in-Chief, Barbagallo, Mario, Editorial Board Member, Çakatay, Ufuk, Editorial Board Member, Fraifeld, Vadim E., Editorial Board Member, Fülöp, Tamàs, Editorial Board Member, Gruber, Jan, Editorial Board Member, Jin, Kunlin, Editorial Board Member, Kaul, Sunil, Editorial Board Member, Kaur, Gurcharan, Editorial Board Member, Le Bourg, Eric, Editorial Board Member, Lopez Lluch, Guillermo, Editorial Board Member, Moskalev, Alexey, Editorial Board Member, Nehlin, Jan, Editorial Board Member, Pawelec, Graham, Editorial Board Member, Rizvi, Syed Ibrahim, Editorial Board Member, Sholl, Jonathan, Editorial Board Member, Stambler, Ilia, Editorial Board Member, Szczerbińska, Katarzyna, Editorial Board Member, Trougakos, Ioannis P., Editorial Board Member, Wadhwa, Renu, Editorial Board Member, Wnuk, Maciej, Editorial Board Member, and Rattan, Suresh I. S., editor

Published
2024
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5. Donepezil-Loaded Nanocarriers for the Treatment of Alzheimer’s Disease: Superior Efficacy of Extracellular Vesicles Over Polymeric Nanoparticles

Author

Oliveira Silva,Rummenigge, Counil,Hermine, Rabanel,Jean-Michel, Haddad,Mohamed, Zaouter,Charlotte, Ben Khedher,Mohamed Raâfet, Patten,Shunmoogum, Ramassamy,Charles, Oliveira Silva,Rummenigge, Counil,Hermine, Rabanel,Jean-Michel, Haddad,Mohamed, Zaouter,Charlotte, Ben Khedher,Mohamed Raâfet, Patten,Shunmoogum, and Ramassamy,Charles

Abstract

Rummenigge Oliveira Silva,1 Hermine Counil,1 Jean-Michel Rabanel,2 Mohamed Haddad,1 Charlotte Zaouter,1 Mohamed Raâfet Ben Khedher,1,3 Shunmoogum A Patten,1 Charles Ramassamy1 1Centre Armand-Frappier Santé Biotechnologie, Institut National de la Recherche Scientifique, Laval, Québec, Canada; 2Faculté de Pharmacie, Université de Montréal, Montréal, Québec, Canada; 3Higher Institute of Biotechnology of Beja, University of Jendouba, Beja, TunisiaCorrespondence: Charles Ramassamy, INRS, Centre Armand-Frappier Santé Biotechnologie, 531 Boul des Prairies, Laval, QC, H7V 1B7, Canada, Tel +450-687 50 10, Email charles.ramassamy@inrs.caIntroduction: Drug delivery across the blood-brain barrier (BBB) is challenging and therefore severely restricts neurodegenerative diseases therapy such as Alzheimer’s disease (AD). Donepezil (DNZ) is an acetylcholinesterase (AChE) inhibitor largely prescribed to AD patients, but its use is limited due to peripheral adverse events. Nanodelivery strategies with the polymer Poly (lactic acid)-poly(ethylene glycol)-based nanoparticles (NPs-PLA-PEG) and the extracellular vesicles (EVs) were developed with the aim to improve the ability of DNZ to cross the BBB, its brain targeting and efficacy.Methods: EVs were isolated from human plasma and PLA-PEG NPs were synthesized by nanoprecipitation. The toxicity, brain targeting capacity and cholinergic activities of the formulations were evaluated both in vitro and in vivo.Results: EVs and NPs-PLA-PEG were designed to be similar in size and charge, efficiently encapsulated DNZ and allowed sustained drug release. In vitro study showed that both formulations EVs-DNZ and NPs-PLA-PEG-DNZ were highly internalized by the endothelial cells bEnd.3. These cells cultured on the Transwell® model were used to analyze the transcytosis of both formulations after validation of the presence of tight junctions, the transendothelial electrical resistance (TEER) values and the permeability of the Dextran-FITC. I

Published
2024

11. Hyperactivation of monocytes and macrophages in MCI patients contributes to the progression of Alzheimer's disease

Author

Munawara, Usma, Catanzaro, Michael, Xu, Weili, Tan, Crystal, Hirokawa, Katsuiku, Bosco, Nabil, Dumoulin, David, Khalil, Abdelouahed, Larbi, Anis, Lévesque, Simon, Ramassamy, Charles, Barron, Annelise E., Cunnane, Stephen, Beauregard, Pascale B., Bellenger, Jean-Pierre, Rodrigues, Serafim, Desroches, Mathieu, Witkowski, Jacek M., Laurent, Benoit, Frost, Eric H., and Fulop, Tamas

Published
2021
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14. Viruses - a major cause of amyloid deposition in the brain

Author

Fulop, Tamas, primary, Ramassamy, Charles, additional, Lévesque, Simon, additional, Frost, Eric H, additional, Laurent, Benoit, additional, Lacombe, Guy, additional, Khalil, Abedelouahed, additional, Larbi, Anis, additional, Hirokawa, Katsuiku, additional, Desroches, Mathieu, additional, Rodrigues, Serafim, additional, Bourgade, Karine, additional, Cohen, Alan A, additional, and Witkowski, Jacek M., additional

Published
2023
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16. Implication of Circulating Extracellular Vesicles-Bound Amyloid-β42 Oligomers in the Progression of Alzheimer's Disease.

Author

Ben Khedher, Mohamed Raâfet, Haddad, Mohamed, Fulop, Tamas, Laurin, Danielle, and Ramassamy, Charles

Subjects
ALZHEIMER'S disease, CEREBRAL amyloid angiopathy, OLIGOMERS, EXTRACELLULAR vesicles, CARRIER proteins, NANOPARTICLES
Abstract

Background: The perplex interrelation between circulating extracellular vesicles (cEVs) and amyloid-β (Aβ) deposits in the context of Alzheimer's disease (AD) is poorly understood. Objective: This study aims to 1) analyze the possible cross-linkage of the neurotoxic amyloid-β oligomers (oAβ) to the human cEVs, 2) identify cEVs corona proteins associated with oAβ binding, and 3) analyze the distribution and expression of targeted cEVs proteins in preclinical participants converted to AD 5 years later (Pre-AD). Methods: cEVs were isolated from 15 Pre-AD participants and 15 healthy controls selected from the Canadian Study of Health and Aging. Biochemical, clinical, lipid, and inflammatory profiles were measured. oAβ and cEVs interaction was determined by nanoparticle tracking analysis and proteinase K digestion. cEVs bound proteins were determined by ELISA. Results: oAβ were trapped by cEVs and were topologically bound to their external surface. We identified surface-exposed proteins functionally able to conjugate oAβ including apolipoprotein J (apoJ), apoE and RAGE, with apoJ being 30- to 130-fold higher than RAGE and apoE, respectively. The expression of cEVs apoJ was significantly lower in Pre-AD up to 5 years before AD onset. Conclusion: Our findings suggest that cEVs might participate in oAβ clearance and that early dysregulation of cEVs could increase the risk of conversion to AD. [ABSTRACT FROM AUTHOR]

Published
2023
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18. Deep Tissue Penetration of Bottle-Brush Polymers via Cell Capture Evasion and Fast Diffusion

Author

Rabanel, Jean-Michel, primary, Mirbagheri, Marziye, additional, Olszewski, Mateusz, additional, Xie, Guojun, additional, Le Goas, Marine, additional, Latreille, Pierre-Luc, additional, Counil, Hermine, additional, Hervé, Vincent, additional, Silva, Rummenigge Oliveira, additional, Zaouter, Charlotte, additional, Adibnia, Vahid, additional, Acevedo, Mariana, additional, Servant, Marc J., additional, Martinez, Vincent A., additional, Patten, Shunmoogum A., additional, Matyjaszewski, Krzysztof, additional, Ramassamy, Charles, additional, and Banquy, Xavier, additional

Published
2022
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24. Date seeds alleviate behavioural and neuronal complications of metabolic syndrome in rats.

Author

Dallagi, Yosra, Rahali, Dalila, Perrotte, Morgane, Dkhili, Houssem, Korsan, Asma, El May, Michele Veronique, El Fazaa, Saloua, Ramassamy, Charles, and El Golli, Narges

Subjects
METABOLIC syndrome, MAZE tests, LIQUID chromatography-mass spectrometry, ORAL drug administration, SPATIAL memory, TROPANES, FAT
Abstract

Unhealthy dietary habits can play a crucial role in metabolic damages, promoting alteration of neural functions through the lifespan. Recently, dietary change has been perceived as the first line intervention in prevention and/or treatment of metabolic damages and related diseases. In this context, our study was designed to assess the eventual therapeutic effect of date seeds administration on memory and learning and on neuronal markers in a rat Metabolic Syndrome model. For this purpose, 32 adult male Wistar rats were fed with standard diet or high-fat high-sugar diet during ten weeks. After this, 16 rats were sacrified and the remaining rats received an oral administration of 300 mg of date seeds/kg of body weight during four supplementary weeks. Before sacrifice, we evaluate cognitive performances by the Barnes maze test. Afterwards, neuronal, astrocytic, microtubular and oxidative markers were investigated by immunoblotting methods. In Metabolic syndrome rats, results showed impairment of spatial memory and histological alterations. We identified neuronal damages in hippocampus, marked by a decrease of NeuN and an increase of GFAP and pTau396. Finally, we recorded an increase in protein oxidation and lipid peroxidation, respectively identified by an up-regulation of protein carbonyls and 4-HNe. Interestingly, date seeds administration improved these behavioural, histological, neuronal and oxidative damages highlighting the neuroprotective effect of this natural compound. Liquid Chromatography-Mass Spectrometry (LC-MS) identified, in date seeds, protocatechuic acid, caffeoylshikimic acid and vanillic acid, that could potentially prevent the progression of neurodegenerative diseases, acting through their antioxidant properties. [ABSTRACT FROM AUTHOR]

Published
2023
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42. Additional file 1 of Hyperactivation of monocytes and macrophages in MCI patients contributes to the progression of Alzheimer's disease

Author

Munawara, Usma, Catanzaro, Michael, Xu, Weili, Tan, Crystal, Hirokawa, Katsuiku, Bosco, Nabil, Dumoulin, David, Khalil, Abdelouahed, Larbi, Anis, Lévesque, Simon, Ramassamy, Charles, Barron, Annelise E., Cunnane, Stephen, Beauregard, Pascale B., Bellenger, Jean-Pierre, Rodrigues, Serafim, Desroches, Mathieu, Witkowski, Jacek M., Laurent, Benoit, Frost, Eric H., and Fulop, Tamas

Abstract

Additional file 1: Supplementary Figure 1. The effect of LPS and BHB on phagocytosis of fluorescent amyloid-beta (Aβ1-42). Monocytes from healthy and MCI patients and microglia cell line HMC3 were cultured as described in the M & M. A) Comparison of resting phagocytosis of fluorescent Aβ1-42 and the effect of BHB, LPS and their combination on fluorescent Aβ1-42 phagocytosis between the microglia, healthy (H) and MCI monocytes. N=7 for each group in duplicate. The exact p values are shown for significant differences. B) Comparison of the effect of BHB, LPS and their combination on fluorescent Aβ1-42 phagocytosis in the microglia, healthy (H) and MCI monocytes. N=7 for each group in duplicate. **** - p

Published
2021
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43. Additional file 3 of Hyperactivation of monocytes and macrophages in MCI patients contributes to the progression of Alzheimer's disease

Author

Munawara, Usma, Catanzaro, Michael, Xu, Weili, Tan, Crystal, Hirokawa, Katsuiku, Bosco, Nabil, Dumoulin, David, Khalil, Abdelouahed, Larbi, Anis, Lévesque, Simon, Ramassamy, Charles, Barron, Annelise E., Cunnane, Stephen, Beauregard, Pascale B., Bellenger, Jean-Pierre, Rodrigues, Serafim, Desroches, Mathieu, Witkowski, Jacek M., Laurent, Benoit, Frost, Eric H., and Fulop, Tamas

Abstract

Additional file 3: Supplementary Figure 3. TLR4 and TLR2 expression in human monocytes at basal level. Flow cytometry analysis of human monocytes in healthy subjects, SMC, MCI, and AD patients, based on the CD284 and CD282 expression pattern. A) TLR4. B) TLR2. Statistical analyses were performed by one-way ANOVA with Dunnett’s multiple comparison tests to assess differences between patient groups. Data are a combination of 18 independent experiments and are shown as mean of MFI ± SD. The ns indicate non-significance.

Published
2021
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44. Additional file 4 of Hyperactivation of monocytes and macrophages in MCI patients contributes to the progression of Alzheimer's disease

Author

Munawara, Usma, Catanzaro, Michael, Xu, Weili, Tan, Crystal, Hirokawa, Katsuiku, Bosco, Nabil, Dumoulin, David, Khalil, Abdelouahed, Larbi, Anis, Lévesque, Simon, Ramassamy, Charles, Barron, Annelise E., Cunnane, Stephen, Beauregard, Pascale B., Bellenger, Jean-Pierre, Rodrigues, Serafim, Desroches, Mathieu, Witkowski, Jacek M., Laurent, Benoit, Frost, Eric H., and Fulop, Tamas

Abstract

Additional file 4: Supplementary Figure 4. Intracellular pro- and anti-inflammatory cytokine production in MDM at basal level. Flow cytometry analysis of human MDM in healthy subjects, SMC, MCI, and AD patients, based on the IL-10, IL-4, IL-1β, IL-6, and TNFα expression pattern. A) IL-10 expression. B) IL-4 expression. C) IL-1β expression. D) IL-6 expression. E) TNFα expression. The data are presented as a mean of MFI ± SD. Data at the basal level are a combination of 12 independent experiments. Statistical analyses were performed by one-way ANOVA with Dunnett’s multiple comparison tests to assess differences between patient groups. The asterisk corresponds to *p

Published
2021
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45. Cerebral Apolipoprotein D exits the brain and accumulates in peripheral tissues

Author

Desmarais, Frederik, Hervé, Vincent, Bergeron, Karl-F., Ravaut, Gaetan, Perrotte, Morgane, Fyfe-Desmarais, Guillaume, Rassart, Eric, Ramassamy, Charles, Mounier, Catherine, Desmarais, Frederik, Hervé, Vincent, Bergeron, Karl-F., Ravaut, Gaetan, Perrotte, Morgane, Fyfe-Desmarais, Guillaume, Rassart, Eric, Ramassamy, Charles, and Mounier, Catherine

Abstract

Apolipoprotein D (ApoD) is a secreted lipocalin associated with neuroprotection and lipid me-tabolism. In rodent, the bulk of its expression occurs in the central nervous system. Despite this, ApoD has profound effects in peripheral tissues, indicating that neural ApoD may reach pe-ripheral organs. We endeavour to determine if cerebral ApoD can reach the circulation and ac-cumulate in peripheral tissues. 3 hours was necessary for over 40% of all the radiolabeled human ApoD (hApoD), injected bilaterally, to exit the CNS. Once in circulation, hApoD accumulates mostly in the kindeys/urine, liver, and muscles. Accumulation specificity of hApoD in these tis-sues was strongly correlated with the expression of lowly glycosylated basigin (BSG, CD147). hApoD was observed to pass through bEnd.3 blood brain barrier endothelial cells monolayers. However, cyclophilin A did not impact hApoD internalisation rates in bEnd.3, indicating that ApoD exit from the brain is either independent of BSG or relies on additional cell types. Overall, our data shows that ApoD can quickly and efficiently exit the CNS and reach the liver and kid-neys/urine, organs linked to the recycling and excretion of lipids and toxins. This indicates that cerebral overexpression during neurodegenerative episodes may serve to evacuate neurotoxic ApoD ligands from the CNS.

Published
2021

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