Introduction

Alzheimer’s disease (AD) is the leading cause of dementia and loss of autonomy and independency in the elderly.1 Currently, no effective pharmacological interventions change the onset or progression of AD.2 Mild cognitive impairment (MCI) is possibly the earliest stage of detectable dementia and may be the optimal time to intervene.3 4 Exploring factors and biochemical markers that are associated with late-life dementia has attracted much attention. A growing body of epidemiological evidence has suggested that deficiency of nutrition components may be related to the development of cognitive decline.5

Vitamin D can play an important role in brain health and function, and exert various neuroprotective effects in brain areas essential for cognition.6 Being severely deficient in vitamin D is associated with a more than twofold increased risk of developing dementia.7 Protective effects of vitamin D on cognition and pathology are also concluded in animal models.8 9Sonnenberg et al 9 found that 1,25-dihydroxyvitamin D (1,25-D) treatment increases choline acetyltransferase activity in specific rat brain nuclei. Supplementation of vitamin D₃ may have contributed to the observed improvements to memory via increasing acetylcholine concentration. Vitamin D research has gained increased attention in recent times due to its roles beyond bone health and calcium homeostasis, such as neurocognitive.10 However, results have been inconclusive.1 11 The mechanisms still remain unclear.

The brain is the most lipid-rich organ in the body,12 and almost all major classes of lipids have some correlation with AD pathogenesis.13 Several population-based studies reported that elderly people with AD or with dementia or cognitive impairment have higher plasma total cholesterol (TC) than sex and age-matched non-demented peers.14–16 Brain and peripheral lipid levels were once thought to be entirely isolated from one another by the blood–brain barrier, but recent evidence …