TY  - JOUR
AB  - BACKGROUND: Iron dysregulation has been implicated in the pathogenesis of dementia, since it is an essential nutrient for neuronal function, but also contributes to oxidative stress and neurotoxicity at elevated levels. METHODS: We enrolled 56 individuals with newly-diagnosed mild cognitive impairment (MCI) and followed over a 47-month period to monitor conversion to dementia according to baseline percentage concentrations of cerebrospinal fluid iron species RESULTS: In this cohort, 28 participants developed Alzheimer's dementia, 5 frontotemporal dementia, 2 Lewy body dementia, and 2 vascular dementia during the follow-up. Higher Fe-Ferritin was associated with a higher though statistically unstable dementia risk (hazard ratio HR 1.36 for 10-unit % increase, 95% confidence interval-CI 0.88-2.11), while Fe-Transferrin was linked to a lower risk (HR 0.65, 95% CI 0.21-2.08) and inorganic Fe showed little association (HR 1.06, 95% CI 0.80-1.40). Patterns of association were non-linear: inorganic Fe had a U-shaped association, with reduced risk at 25-40% and increased risk above 45%; Fe-Ferritin showed an inverted U-shape relation with higher risk between 10-20%; Fe-Transferrin showed almost no relation with dementia risk. When considering conversion to Alzheimer's dementia only, the relation was similarly U-shaped for inorganic Fe and almost null for Fe-Transferrin, while Fe-Ferritin showed a positive relation with risk above 15%. CONCLUSIONS: Despite the statistical imprecision of the estimates, our study provides novel evidence linking iron species in cerebrospinal fluid to dementia risk in individuals with MCI. These findings also underscore the importance of elemental speciation in dementia research.
AU  - Urbano, T.*
AU  - Michalke, B.
AU  - Chiari, A.*
AU  - Malagoli, C.*
AU  - Bedin, R.*
AU  - Tondelli, M.*
AU  - Vinceti, M.*
AU  - Filippini, T.*
C1  - 75070
C2  - 57788
CY  - Radarweg 29, 1043 Nx Amsterdam, Netherlands
TI  - Iron species in cerebrospinal fluid and dementia risk in subjects with mild cognitive impairment: A cohort study.
JO  - Neurotoxicol.
VL  - 110
PB  - Elsevier
PY  - 2025
SN  - 0161-813x
ER  - 

TY  - JOUR
AB  - Exposure to selenium, and particularly to its inorganic forms, has been hypothesized as a risk factor for amyotrophic lateral sclerosis (ALS), a fast progressing motor neuron disease with poorly understood etiology. However, no information is known about levels of inorganic and some organic selenium species in the central nervous system of ALS patients, and recent observations suggest that peripheral biomarkers of exposure are unable to predict these levels for several Se species including the inorganic forms. Using a hospital-referred case-control series and advanced selenium speciation methods, we compared the chemical species of selenium in cerebrospinal fluid from 38 ALS patients to those of 38 reference neurological patients matched on age and gender. We found that higher concentrations of inorganic selenium in the form of selenite and of human serum albumin-bound selenium were associated with increased ALS risk (relative risks 3.9 (95% confidence interval 1.2-11.0) and 1.7 (1.0-2.9) for 0.1μg/L increase). Conversely, lower concentrations of selenoprotein P-bound selenium were associated with increased risk (relative risk 0.2 for 1μg/L increase, 95% confidence interval 0.04-0.8). The associations were stronger among cases age 50 years or older, who are postulated to have lower rates of genetic disease origin. These results suggest that excess selenite and human serum albumin bound-selenium and low levels of selenoprotein P-bound selenium in the central nervous system, which may be related, may play a role in ALS etiology.
AU  - Vinceti, M.*
AU  - Solovyev, N.
AU  - Mandrioli, J.*
AU  - Crespi, C.M.*
AU  - Bonvicini, F.*
AU  - Arcolin, E.*
AU  - Georgoulopoulou, E.*
AU  - Michalke, B.
C1  - 25174
C2  - 31842
SP  - 25-32
TI  - Cerebrospinal fluid of newly diagnosed amyotrophic lateral sclerosis patients exhibits abnormal levels of selenium species including elevated selenite.
JO  - Neurotoxicol.
VL  - 38
PB  - Elsevier Science
PY  - 2013
SN  - 0161-813x
ER  -