Although recent studies suggest homocysteine (Hcy) is an independent risk factor for neurodegenerative disorders, little is known about sex differences in the levels of Hcy. In this study, we conducted a comparative meta-analysis to investigate sex differences in the levels of Hcy in both Alzheimer’s disease (AD) and Parkinson’s disease (PD) patients. Reports of Hcy stratified by sex in both AD and PD patients were obtained from electronic databases. From the initial 1595 records, 921 were assessed for eligibility, of which 16 sufficiently reported sex differences. Standardized mean difference (SMDs) using random effects together with tests of heterogeneity and quality assessment were applied in this meta-analysis. Data from 3082 diagnosed patients (1162 males and 1920 females) were included. There were statistically significant differences in the levels of Hcy between sexes in AD and PD patients, with an SMD of 0.291 [0.17, 0.41], p < 0.05, 95% CI, with higher Hcy levels detected in males. Subgroup comparisons did not find a statistically significant difference in the levels of Hcy between AD and PD patients. The overall risk of bias for the analyzed studies was low, with some moderate risk of bias across select domains. This meta-analysis determined that compared to females, males with either AD or PD have higher levels of Hcy. These findings suggest that Hcy could be a useful biomarker for predicting neurodegenerative diseases in males; however, further studies are needed to confirm the clinical utility of this suggestion.
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder that debilitates over 55 million individuals worldwide. Currently, treatments manage and alleviate its symptoms; however, there is still a need to find a therapy that prevents or halts disease progression. Since AD has been labeled as “type 3 diabetes” due to its similarity in pathological hallmarks, molecular pathways, and comorbidity with type 2 diabetes mellitus (T2DM), there is growing interest in using anti-diabetic drugs for its treatment. Rosiglitazone (RSG) is a peroxisome proliferator-activated receptor-gamma agonist that reduces hyperglycemia and hyperinsulinemia and improves insulin signaling. In cellular and rodent models of T2DM-associated cognitive decline and AD, RSG has been reported to improve cognitive impairment and reverse AD-like pathology; however, results from human clinical trials remain consistently unsuccessful. RSG has also been reported to modulate the expression of brain-derived neurotrophic factor (BDNF), a protein that regulates neuroplasticity and energy homeostasis and is implicated in both AD and T2DM. The present review investigates RSG’s limitations and potential therapeutic benefits in pre-clinical models of AD through its modulation of BDNF expression.
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