Abstract
BackgroundLittle is known about factors influencing progression from mild cognitive impairment to Alzheimer’s dementia. A potential role of environmental chemicals and specifically of selenium, a trace element of nutritional and toxicological relevance, has been suggested. Epidemiologic studies of selenium are lacking, however, with the exception of a recent randomized trial based on an organic selenium form.MethodsWe determined concentrations of selenium species in cerebrospinal fluid sampled at diagnosis in 56 participants with mild cognitive impairment of nonvascular origin. We then investigated the relation of these concentrations to subsequent conversion from mild cognitive impairment to Alzheimer’s dementia.ResultsTwenty-one out of the 56 subjects developed Alzheimer’s dementia during a median follow-up of 42 months; four subjects developed frontotemporal dementia and two patients Lewy body dementia. In a Cox proportional hazards model adjusting for age, sex, duration of sample storage, and education, an inorganic selenium form, selenate, showed a strong association with Alzheimer’s dementia risk, with an adjusted hazard ratio of 3.1 (95% confidence interval 1.0–9.5) in subjects having a cerebrospinal fluid content above the median level, compared with those with lower concentration. The hazard ratio of Alzheimer’s dementia showed little departure from unity for all other inorganic and organic selenium species. These associations were similar in analyses that measured exposure on a continuous scale, and also after excluding individuals who converted to Alzheimer’s dementia at the beginning of the follow-up.ConclusionsThese results indicate that higher amounts of a potentially toxic inorganic selenium form in cerebrospinal fluid may predict conversion from mild cognitive impairment to Alzheimer’s dementia.
Highlights
Little is known about factors influencing progression from mild cognitive impairment to Alzheimer’s dementia
When we assessed the correlation between Se species, the only forms not associated with total Se were Se(VI), Glutathione-peroxidase-bound Se (Se-GPX), and selenocysteinebound Se (Se-Cys), the latter form being unrelated to total organic Se
All correlations involving Se-Cys and especially Se-GPX were based on a small number of individuals, because a large proportion of the sample concentrations fell below the limit of detection (LOD)
Summary
Little is known about factors influencing progression from mild cognitive impairment to Alzheimer’s dementia. Among the large number of chemical factors that have been implicated in the etiology of dementia, its most common form, Alzheimer’s dementia (AD), recent concern has focused on both increased and decreased exposure to the metalloid selenium (Se), an element of strong nutritional and toxicological interest [5,6,7,8]. Its involvement in human brain pathology, and with the risk of amyotrophic lateral sclerosis and AD, has become a focus [17, 23,24,25,26,27,28,29] Such a relation, may exist only for some Se species, and for the inorganic ones [30, 31]
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