Background: Mild cognitive impairment (MCI) has an increased rate of progression to dementia.
Alterations of some metabolic factors, such as deficiency of vitamin D, are a risk factor for cognitive
deterioration. Vitamin D is involved in the clearance of β-amyloid (Aβ) from the brain. We have
reported that lymphocytes from Alzheimer's disease (AD) patients have an increased susceptibility to
oxidative death by H2O2 exposure, but currently it is unknown if this characteristic is modifiable in vivo.
Objective: To determine if correction of low vitamin D levels protects lymphocytes from oxidative death
and increases Aβ1-40 plasma levels in MCI and very early AD (VEAD) patients.
Method: Sixteen MCI, 11 VEAD and 25 healthy control (HC) voluntaries were evaluated with the
Clinical Dementia Rating (CDR), Montreal Cognitive assessment (MoCA), and Memory Index score
(MIS). Lymphocyte death was measured by flow cytometry after 20h exposure to H2O2. In patients with
low levels of vitamin D -11 MCI, 9 VEAD and 20 HC- lymphocyte H2O2-death, plasma Aβ1-40 levels
and cognitive status were evaluated pre- and post-vitamin D supplementation for 6 months.
Results: Lymphocytes from MCI and VEAD patients showed increased susceptibility to oxidative death
at study entry. In MCI, but not VEAD patients, lymphocyte susceptibility to death and Aβ1-40 levels
plasma levels improved after 6 months of vitamin D supplementation. In addition, cognitive status on
follow-up (18 months) improved in MCI patients after vitamin D supplementation.
Conclusion: Vitamin D supplementation may be beneficial in MCI. The lack of effect in VEAD may be
due to a more advanced stage or different characteristics of the neurodegenerative process.