Alzheimer’s disease (AD) is the most common form of dementia, in which progressive amyloid plaques strangle the brain. There is no cure for the disease, which worsens with time and eventually leads to death. In the early stages of AD, the most common symptom is difficulty in remembering recent events. As the disease advances, symptoms can include confusion, irritability and aggression, mood swings, trouble with language, and long-term memory loss. As the sufferer declines, they often withdraw from family and society. Gradually, bodily functions are lost, ultimately leading to death.
The vast majority of AD cases are sporadic, meaning that they are not directly inherited, although some genes act as risk factors. Only 0.1% of the cases are predictably inherited (autosomal dominate) and usually occur before age 65. However, there are clear genetic risk factors and the best-known genetic risk factor is the inheritance of APOE gene. Between 40% and 80% of people with AD possess at least one APOE gene. The APOE gene increases the risk of the disease by 3 times in those with one copy of the gene and by 15 times in those with two copies of the gene. However, this “genetic” effect is not necessarily purely genetic. For example, certain equatorial populations (Nigerian) show no relationship between presence of the APOE gene and AD. Geneticists agree that evidence indicates a strong role for unknown environmental effects.
AD is rapidly increasing. In the United States, AD prevalence was almost 2% of the total population in 2000, with the rate as high as 19% in 75–84 year olds, and 42% in the greater than 84 year olds. Prevalence rates in less developed regions of the world are lower. A study estimated that in 2006, 27 million people in the world were afflicted with AD, and that the prevalence rate would triple and the absolute number would quadruple by the year 2050 given the increasing rates and growing population.
What is the environmental factor? Recently, Doctor Cedric Annweiler and colleagues of the University of Angers in France reviewed all the studies on vitamin D and Alzheimer’s. Could vitamin D be a big piece to the puzzle?
They reviewed 284 selected studies, to find nine case-controlled studies and one cohort study that met their selection criteria. The pooled effect size in random-effects meta-analysis was 1.40, a ‘large’ effect size that indicates that serum 25OHD concentrations were 1.40 standard deviation units lower in AD cases compared to cognitively healthy controls. In other words, people suffering from AD are much more likely to be deficient in vitamin D than people without AD.
They concluded there were two main possibilities. One, that patients with AD were less likely to go outside into the sunshine, or that low 25(OH)D was an environmental risk factor for AD. For a number of reasons, they thought the first possibility is less likely than the second one.
They also reviewed the literature to find a number of ways that vitamin D helps the brain. Although the exact basis of AD is not fully understood, different mechanisms of nerve death have emerged, including deposition of amyloid plaques, inflammatory processes, neuronal tangles, glutamate toxicity, excessive intracellular calcium levels, and oxidative stress .
In regards to vitamin D, they found evidence in their review that:
The authors concluded,
“This experimentally proved involvement of vitamin D in brain pathways, together with the present finding that serum vitamin D concentrations are overall lower in AD compared to controls, sheds new light on the possible involvement of vitamin D in the course of AD.”