Selenium Neuroprotection in Neurodegenerative Disorders

Effects of Selenium Supplementation in Patients with Mild Cognitive Impairment or Alzheimer’s Disease: A Systematic Review and Meta-Analysis

“…Se is an essential element for the maintenance of mammalian life and a component of selenoproteins, which are part of the endogenous antioxidant system. The brain is particularly dependent on Se supply, and is spared from Se deficiency [ 1 , 7 ]. Moreover, Se is important for the protection against oxidative stress [ 37 ] and inflammatory processes [ 38 ].…”

“…Selenium (Se) is a trace element that can be found naturally in inorganic (e.g., selenite and selenate) or organic (e.g., selenocysteine and selenomethionine) chemical forms [ 1 , 2 , 3 , 4 , 5 ]. Se is essential for human health because it is part of selenoproteins, which participate in antioxidant and anti-inflammatory pathways [ 1 , 6 , 7 ]. Se is pivotal for human development and plays a significant role in the central nervous system [ 1 , 6 ].…”

“…Se is pivotal for human development and plays a significant role in the central nervous system [ 1 , 6 ]. Several studies in rodents have demonstrated that the depletion of some selenoproteins, such as selenoprotein P (SELP), causes irreversible brain damage, predisposition to seizures, impaired motor coordination, and cognitive decline [ 7 , 8 , 9 ]. Interestingly, Rueli et al [ 10 ] demonstrated that SELP is significantly increased in the choroid plexus and cerebrospinal fluid of patients with Alzheimer’s disease (AD); on the other hand, Garlet et al [ 11 ] observed a decrease in blood glutathione peroxidase (GPX) activity in AD patients.…”

“…Described in 1907 by the German neuropathologist Alois Alzheimer, AD is a progressive neurodegenerative disease that manifests itself with reduced cognitive ability and memory loss, being one of the most common forms of dementia. It is characterized by the existence of neurofibrillary tangles containing β-amyloid peptide and tau protein in the pathological brain tissue, leading to neuronal degeneration [ 7 , 12 , 13 ]. Moreover, its pathophysiology is related to the large production of reactive oxygen species, inflammatory markers, decreased antioxidant agents, and brain metabolic changes [ 7 , 12 , 13 , 14 ].…”

“…It is characterized by the existence of neurofibrillary tangles containing β-amyloid peptide and tau protein in the pathological brain tissue, leading to neuronal degeneration [ 7 , 12 , 13 ]. Moreover, its pathophysiology is related to the large production of reactive oxygen species, inflammatory markers, decreased antioxidant agents, and brain metabolic changes [ 7 , 12 , 13 , 14 ].…”