Diabetes, Alzheimer disease, and vascular dementia: A population-based neuropathologic study

Neurology ◽  
2010 ◽  
Vol 75 (13) ◽  
pp. 1195-1202 ◽  
Author(s):  
S. Ahtiluoto ◽  
T. Polvikoski ◽  
M. Peltonen ◽  
A. Solomon ◽  
J. Tuomilehto ◽  
...  
2015 ◽  
Vol 11 (7S_Part_14) ◽  
pp. P652-P653
Author(s):  
Arianna Romani ◽  
Eleonora Cremonini ◽  
Carlo Cervellati ◽  
Cristina Bosi ◽  
Monica Squerzanti ◽  
...  

2005 ◽  
Vol 77 (4) ◽  
pp. 643-652 ◽  
Author(s):  
Rosa Rademakers ◽  
Marc Cruts ◽  
Kristel Sleegers ◽  
Bart Dermaut ◽  
Jessie Theuns ◽  
...  

1996 ◽  
Vol 53 (5) ◽  
pp. 436-439 ◽  
Author(s):  
J. G. Buckwalter ◽  
A. A. Rizzo ◽  
R. McCleary ◽  
R. Shankle ◽  
M. Dick ◽  
...  

2021 ◽  
Vol 79 (4) ◽  
pp. 1601-1612
Author(s):  
Johan Frederik Håkonsen Arendt ◽  
Erzsébet Horváth-Puhó ◽  
Henrik Toft Sørensen ◽  
Ebba Nexø ◽  
Lars Pedersen ◽  
...  

Background: It is controversial whether B12 deficiency causes dementia or B12 treatment can prevent dementia. Objective: To assess associations between low plasma (P-)B12 levels, B12 treatment, and risk of Alzheimer’s disease (AD; primary outcome) and all-cause or vascular dementia (secondary outcomes). Methods: We conducted a population-based cohort study using Danish registry data to assess associations between low P-B12 levels, high-dose injection or oral B12 treatment, and risk of dementia (study period 2000–2013). The primary P-B12 cohort included patients with a first-time P-B12 measurement whose subsequent B12 treatment was recorded. The secondary B12 treatment cohort included patients with a first-time B12 prescription and P-B12 measurement within one year before this prescription. For both cohorts, patients with low P-B12 levels (<200 pmol/L) were propensity score-matched 1:1 with patients with normal levels (200–600 pmol/L). We used multivariable Cox regression to compute 0–15-year hazard ratios for dementia. Results: For low P-B12 and normal P-B12 level groups, we included 53,089 patients in the primary P-B12 cohort and 13,656 patients in the secondary B12 treatment cohort. In the P-B12 cohort, hazard ratios for AD centered around one, regardless of follow-up period or treatment during follow-up. In the B12 treatment cohort, risk of AD was unaffected by low pre-treatment P-B12 levels, follow-up period and type of B12 treatment. Findings were similar for all-cause and vascular dementia. Conclusion: We found no associatio1n between low P-B12 levels and dementia. Associations were unaffected by B12 treatment. Results do not support routine screening for B12 deficiency in patients with suspected dementia.


1997 ◽  
pp. 13-17 ◽  
Author(s):  
Helena Chui ◽  
Qian Zhang ◽  
Jeff Victoroff ◽  
Barbara Zaias

2006 ◽  
Vol 81 (10) ◽  
pp. 1350-1358 ◽  
Author(s):  
Martin R. Farlow

2010 ◽  
Vol 6 (3) ◽  
pp. 124-124
Author(s):  
Eleanor Beal

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