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1.
Nutr Neurosci ; : 1-8, 2024 Mar 14.
Article in English | MEDLINE | ID: mdl-38486449

ABSTRACT

Background: The Mediterranean diet has been linked to brain neuroprotection. Evidence from meta-analyses showed reduced risk of dementia with greater intake of vegetables and fruits, fish, and the Mediterranean diet. The current study raises important questions about the association between low risk dementia and Mediterranean diet.Objective: The objective was to evaluate the association between levels of adherence to the Mediterranean diet and dementia and cognitive status in subjects 50 years of age and older.Method: The Mediterranean Diet Adherence Screener (MEDAS), the modified 30-item 'Diagnostic and Statistical Manual of Mental Disorders Third Edition (DSM-III) risk of dementia, and the Standard Mini-Mental Status Examination (SMMSE) cognitive status scores were used to assess the levels of adherence to the Mediterranean diet'.Results: A total of 150 subjects were enrolled in the study. Forty-one (27.3%) had 'suspected or confirmed dementia, while 48 individuals (32%) were categorized as having moderate to severe cognitive decline. Subjects who reported moderate to high adherence to the Mediterranean diet (55, 36.7%) had significantly lower dementia scores (7.0 3.8 versus 17.6 5.1) and higher cognitive (25.4 3.8 versus 8.6 7.2) scores compared to those (38, 25.3%) who reported low adherence to the Mediterranean diet.Conclusion: Subjects who were highly or moderately adherent to the Mediterranean diet had significantly lower dementia scores and better cognitive status than those with low adherence.

2.
Saudi Pharm J ; 31(12): 101871, 2023 Dec.
Article in English | MEDLINE | ID: mdl-38125952

ABSTRACT

Background: Huntington's disease is an inherited progressive neurodegenerative disorder caused by an expansion of the polyglutamine tract leading to malformation and aggregation of the mutant huntingtin protein in the cell cytoplasm and nucleus of affected brain regions. The development of neuroprotective agents from plants has received considerable research attention. Objective: Our study aims to investigate the neuroprotective effects of luteolin and the mechanisms that underline its potential mediated protection in the mutant htt neuroblastoma cells. Methods: The mutant htt neuroblastoma cells were transfected with 160Q, and the control wild-type neuroblastoma cells were transfected with 20Q htt for 24 h and later treated with luteolin. Cell viability was determined by MTT and PI staining in both groups, while western blotting was used to evaluate caspase 3 protein expression. Aggregation formation was assessed via immunofluorescence microscopy. Also, western blotting was utilized to measure the protein expression of mutant htt aggregated and soluble protein, Nrf2 and HO-1. The impact of Nrf2 on luteolin-treated neuroblastoma cells was assessed using small interfering RNAs. Results: Our study reports that luteolin can protect cultured cells from mutant huntingtin cytotoxicity, evidenced by increased viability and decreased apoptosis. Also, luteolin reduced the accumulation of soluble and insoluble mutant huntingtin aggregates in mutant htt neuroblastoma cells transfected with 160Q compared to the control wild-type. The mutant htt aggregate reduction mediated by luteolin appeared to be independent of the Nrf2 -HO-1 antioxidant pathway. Conclusion: Luteolin presents a new potential therapeutic and protective agent for the treatment and decreasing the cytotoxicity in neurodegenerative diseases such as Huntington's disease.

3.
Curr Rev Clin Exp Pharmacol ; 18(1): 64-87, 2023.
Article in English | MEDLINE | ID: mdl-35114930

ABSTRACT

BACKGROUND: The current therapy of Rheumatoid Arthritis (RA) is confronted with many challenges such as inadequate response, infection, and treatment failure. AIM AND OBJECTIVE: The main objective was to assess the efficacy and safety of tocilizumab (TCZ) in subjects with RA using the available evidence from published randomized controlled trials. METHODS: The current systematic review was performed on nine randomized controlled trials from 2002 to 2016 for TCZ in subjects with rheumatoid arthritis. The primary outcomes were the clinical improvement in American College Rheumatology 20% (ACR20) or Disease Activity Score remission (DAS28), in addition to other outcomes such as ACR50 and ACR70 in the intention-to-treat population. RESULTS: We have conducted a systematic review on nine randomized controlled trials, with 4129 [100%] enrolled, of which 3248 [78.7%] were on the intention-to-treat. 2147 (66.1%) were treated with TCZ and 1101 (33.9%) have had received placebo or methotrexate or other conventional Disease- Modifying Anti-rheumatic Drugs (cDMARD) or biologic Disease-Modifying Anti-rheumatic Drugs (bDMARDs). In subjects taking TCZ with or without concomitant methotrexate, compared to placebo, subjects treated with TCZ 4 or 8 mg/kg were substantially and statistically significantly more likely than placebo or methotrexate to achieve the ACR20 and/or DAS28. There were no statistically significant differences in serious adverse events such as serious infection; however, subjects on TCZ were more likely to have increased lipid profiles. CONCLUSION: TCZ mono-therapy or in combination with methotrexate is valuable in diminishing rheumatoid arthritis disease activity and improving disability. Treatment with TCZ was associated with a significant surge in cholesterol levels but no serious adverse effects. Randomized clinical trials with safety as the primary outcome are warranted to report these safety issues.


Subject(s)
Antirheumatic Agents , Arthritis, Rheumatoid , Humans , Methotrexate/adverse effects , Randomized Controlled Trials as Topic , Arthritis, Rheumatoid/drug therapy , Antirheumatic Agents/adverse effects
4.
Curr Rev Clin Exp Pharmacol ; 18(2): 120-147, 2023.
Article in English | MEDLINE | ID: mdl-35642121

ABSTRACT

BACKGROUND: A subpopulation of statin users such as subjects with chronic kidney disease (CKD), Human Immune virus (HIV), acute coronary syndrome (ACS), revascularization, metabolic syndrome, and/or diabetes may particularly benefit from pitavastatin pharmacotherapy. AIM: The current systematic review aimed systematically to evaluate the effect of pitavastatin on primary cardiac events in subjects receiving pitavastatin in comparison to the other four statin members. METHODS: We conducted a systematic review on phases III and IV of randomized controlled trials (RCT-s, 11 trials) for subjects with primary cardiac events who received pitavastatin. Subjects diagnosed with any type of dyslipidemia (population 4804) and received pitavastatin (interventions) versus comparator (comparison) with the primary efficacy endpoint of minimization of LDL-C and non- HDL-C, had an increase in HDL-C and/or reduction in major adverse cardiac events (MACE, cardiovascular death, myocardial infarction (fatal/nonfatal), and stroke (fatal/nonfatal) and/or their composite (outcomes). The secondary safety endpoint was the development of any adverse effects. RESULTS: In the included trials (11), participants (4804) were randomized for pitavastatin or its comparators such as atorvastatin, pravastatin, rosuvastatin, simvastatin and followed up for 12 to 52 weeks. In terms of the primary outcome (reduction in LDL-C), pitavastatin 4 mg was superior to pravastatin 40 mg in three trials, while the 2 mg pitavastatin was comparable to atorvastatin 10 mg in four trials and simvastatin 20 and 40 mg in two 2 trials. However, rosuvastatin 2.5 mg was superior to pitavastatin 2 mg in two trials. Pitavastatin increased HDL-C and reduced non-HDL-C in eleven trials. Regarding the safety profile, pitavastatin has proved to be tolerated and safe. CONCLUSION: The FDA-approved indications for pitavastatin included primary dyslipidemia and mixed dyslipidemia as a supplementary therapy to dietary changes to lower total cholesterol, LDL-C, apolipoprotein B (Apo B), triglycerides (TG), and enhance HDL-C. Pitavastatin might be suitable for subjects with diabetes, ACS (reduced revascularization), metabolic syndrome, CKD, HIV, and subjects with low levels of HDL-C. We highly recommend rational individualization for the selection of statin.


Subject(s)
Cardiovascular Diseases , Dyslipidemias , HIV Infections , Hydroxymethylglutaryl-CoA Reductase Inhibitors , Metabolic Syndrome , Humans , Hydroxymethylglutaryl-CoA Reductase Inhibitors/adverse effects , Atorvastatin/therapeutic use , Rosuvastatin Calcium/therapeutic use , Pravastatin/therapeutic use , Cholesterol, LDL/therapeutic use , Metabolic Syndrome/chemically induced , Cholesterol, HDL/therapeutic use , Randomized Controlled Trials as Topic , Simvastatin/therapeutic use , Dyslipidemias/drug therapy , Cardiovascular Diseases/drug therapy , HIV Infections/complications
5.
J Pharm Bioallied Sci ; 14(2): 81-92, 2022.
Article in English | MEDLINE | ID: mdl-36034490

ABSTRACT

Background: It would be rational to describe the pattern of the clinical characteristics of the survivors and the nonsurvivors during the critical intensive-infection era of coronavirus disease 2019 (COVID-19). The explicit objective of the current scoping review was to delineate the predictive risk factors associated with case fatality rate (CFR). Methods: Six retrospective studies of subjects infected with COVID-19 published between December 1, 2020, and March 30, 2020, describing nonsurvivors in Wuhan/Hubei, China, were identified. Results: There were 1769 subjects with a mean age of 52 years, and 65.9% were male. The highest comorbidity reported was cardiovascular diseases at 22.2% (393/1769). The overall number of cases admitted to the intensive care unit was 228 (12.9%). The reported overall CFR was 7.7% (136/1769), with the highest at 28.2% (54/191), and the lowest at 1.4% (15/1099). The mean duration of onset until death for nonsurvivors was 15.3 days. Conclusion: We have found that older age, male gender, the longer duration from onset till death (days), development of acute respiratory distress syndrome/shock, preexisting diabetes, and preexisting cardiovascular diseases were the major risk factors associated with high CFR.

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