Association of Selenium Levels with Neurodegenerative disease: A Systemic Review and Meta-analysis

Abstract

Background Neurodegenerative diseases are debilitating and incurable disorders with a rapid-rising prevalence. Selenium, a trace element, works in anti-oxidant and anti-inflammatory aspects through selenoprotein biologically. Nowadays, it is in a great urgency to discover the intrinsic relationship between selenium and neurodegenerative diseases, and find more effective therapeutic strategies to combat these devastating diseases. Method Five public databases including PubMed, Web of Science, EMBASE, Cochrane, Clinical Trials were searched in our research. Random model effects were chosen, and Higgins inconsistency analyses (I2), Cochrane’s Q test, Tau2 were calculated to evaluate the heterogeneity. Result The association of selenium in neurodegenerative diseases patients including Alzheimer’s disease, Parkinson’s disease, Multiple sclerosis, Amyotrophic lateral sclerosis and Huntington’s disease was studied. The strong relation was only found in AD patients, especially the erythrocytes in sub-group analysis of various tested tissue type. Conclusion Generally, this meta-analysis indicated that Alzheimer’s disease is strongly associated with lower selenium concentration, which may provide clinical reference in the future. However, more researches are in urgent need for further study and treatment for neurodegenerative diseases.

Association between Parkinson disease and selenium levels in the body: A systematic review and meta-analysis

“…Recent studies exploring the therapeutic effects of selenium on alpha-synuclein aggregation in the substantia nigra pars compacta offer promising insights. [8,9] Selenium, through its incorporation into selenoproteins, plays a critical role in mitigating oxidative stress, which is implicated in the pathogenesis of PD. The potential of selenium to influence the aggregation of alpha-synuclein, a key pathological feature of PD, highlights its relevance not only as a trace element of interest but also as a possible therapeutic agent.…”

“…[6,7] This dual capacity underscores the significance of selenium in the neurodegenerative process and supports the investigation into its levels in PD patients. [8] Furthermore, diagnostic criteria for PD emphasize clinical symptoms and advanced diagnostic tools, underscoring the importance of distinguishing PD from other neurodegenerative disorders through biomarkers and neuroimaging, reflecting the multifaceted nature of PD diagnosis and the potential of inflammation-focused research to illuminate novel therapeutic targets. [9,10] Nevertheless, burgeoning research posits an intriguing hypothesis that perturbations in trace element equilibrium could be pivotal in the initiation and progression of PD.…”

SELENOK-dependent CD36 palmitoylation regulates microglial functions and Aβ phagocytosis

“…Patients with AD and APOE4 allele carriers show reduced levels of selenium (Se), an essential trace element, indicating a significant correlation between Se levels and AD [ [6] , [7] , [8] , [9] ]. Therapeutic strategies harnessing Se-centric compounds have yielded promising results in decelerating Aβ and tau pathological progression, restoring synaptic deficits, and ameliorating cognitive impairments in AD models [ [10] , [11] , [12] , [13] , [14] ].…”