A new study has found that in a mouse model of Alzheimer’s disease (AD), supplementation with activated vitamin D reduces the amount of amyloid-beta plaques in the brain and improves cognition.
Amyloid-beta (Aβ) is a type of peptide (a group of amino acids) that forms the main component of amyloid plaques, which are found in relatively high amounts in the brains of patients with AD. These plaques are considered to play an important role in the development and progression of AD.
Observational research has revealed that patients with AD have lower levels of vitamin D and that people with higher levels of vitamin D are less likely to develop the disease. The few clinical trials performed in patients with AD have found conflicting results on the role of vitamin D. However, the sample sizes of these studies were small and a couple of them lacked adequate controls.
Studies have also found that patients with AD have a decreased amount of vitamin D receptors in their hippocampus, which is a component of the brain that is involved in converting short-term memories to long-term memories.
In a recent study, researchers out of Canada looked at mice predisposed to develop amyloid plaques in their brain to serve as a model of AD.
Studying mice allowed the researchers to take a detailed look at the brain after the study concluded to accurately examine the effects of vitamin D supplementation on the accumulation of amyloid plaques.
The researchers separated the mice into either a group that received a placebo injection or a group that was given an injection of calcitriol (100 IU/kg of body weight) four times a day on every other day for eight weeks.
Calcitriol is the activated form of vitamin D that is able to bind to the vitamin D receptor and affect change in cells and tissues. The majority of studies use a form of vitamin D that needs to go through two conversions in order to become calcitriol.
At baseline and after the eight weeks, the researchers also assessed learning and memory as markers of cognition. To do so, they used fear conditioning to determine the amount of freezing behavior. Freezing behavior is the behavior a prey animal displays when they are exposed to certain stimuli, such as a predatory animal, and is characterized by the prey animal ceasing all movement and feigning death.
Did supplementation with activated vitamin D reduce Aβ levels and improve cognition in these mice? Here is what the researchers found:
The researchers interpreted the entirety of the results to mean,
“VDR activation [by calcitriol] during the period of plaque formation decreases the soluble Aβ load and reduces plaque formation in younger TgCRND8 mice, improving conditioned fear memory, confirming that decreasing cerebral Aβ load in these younger mice delays the progression and intensity of AD-like symptoms, as found by others in Tg2576 mice.”
These results are exciting because a reduction of Aβ levels and amyloid plaques actually translated into improved cognition, as measured by improved fear conditioned memory. However this excitement is tempered by the fact that the study was performed in mice and may not generalize to humans.
This study needs to be followed by more clinical trials in AD patients that utilize larger sample sizes and adequate dosages.