Vitamin D deficiency a risk factor for cognitive decline and dementia

12 December 2018



Low levels of vitamin D are linked to the size of a part of the brain crucial to memory formation, research at QBI has shown.

Associate Professor Thomas Burne from the University’s Queensland Brain Institute (QBI) and his team studied the effect of vitamin D deficiency on people’s cognitive performance as well as the volume and function of the hippocampus, a key structure of the brain for formation of memory which is typically found to be much smaller in people diagnosed with dementias.

Using sophisticated equipment from UQ's Centre for Advanced Imaging, Associate Professor Burne and colleagues were able to analyse the structure of these brain cells and how well they connected (and therefore communicated) from data of people diagnosed with mild cognitive impairment.

“The results show that if you have mild cognitive impairment, you’re older, and you have lower vitamin D levels, it’s associated with a smaller hippocampus, disrupted hippocampal network, and worse performance on cognitive tests,” Associate Professor Burne said.

“The questions is, what do you do to prevent that?”

Vitamin D a preventative, not a treatment

Associate Professor Burne emphasised that correcting vitamin D levels should be viewed as a preventative measure rather than a treatment for the onset of brain diseases and disorders.

“We’re thinking that vitamin D is neuroprotective, which means it’s less about treatment, and more about prevention or early intervention to delay the onset of mild cognitive impairment in the first place,” he said.

“I think of it like wearing a seatbelt: if you’re in a car and you crash without your seatbelt on, and then you put your seatbelt on afterwards, it doesn’t really help. You need the seatbelt on before you have the crash to prevent damage. We think the same goes for vitamin D.

“I’ve yet to see a study to show that if you supplement people with dementia with vitamin D, it then restores reduced brain volume to control levels.

“The best evidence is that it slows disease progression, which is still a good thing," he said. "If you could stop people at mild cognitive impairment and don’t allow them to then proceed to get full-on dementia, it would make an impact on quality of life."

“But I think at the moment we understand that it puts the brakes on – it doesn’t actually restore function,” he said.

Right hemisphere more affected than left

An unexpected finding from the study was that the right hippocampus was more affected by vitamin D deficiency than the left by disruption to the way neurons connect to each other.

“We don’t know exactly what’s going on. One idea may be that because most people are right-handed, it could be an asymmetry involved with that, or it could be different levels of plasticity or network function between the hemispheres.”

“But the worrying finding is that we found the exact same thing in our mice – the hippocampal disruption was in the right hemisphere, which was interesting, as mice aren’t predominantly right-handed, or right-pawed" he said.”

 “It’s an unusual finding, but other people have found it too. We still don’t fully understand why it happens.”

Paving the way for future studies

While the study demonstrates a link between a smaller hippocampus and poorer brain cell function with vitamin D deficiency, Associate Professor Burne says future research is needed to understand the mechanisms that drive this effect.

 “The data we’re collecting supports the idea that vitamin D deficiency makes diseases such as dementia, Alzheimer’s, and mild cognitive impairment worse," he said. "But because we don’t understand the exact mechanism, it’s hard to figure out exactly what’s going on.”

The reserach was published in the journal, Human Brain Mapping.

Associate Professor Burne and his research team are currently working on a mouse-model to examine the detailed biological mechanisms. 


The research was funded by an NHMRC project grant to Thomas Burne and a University of Queensland International PhD Scholarship to Mamun Al-Amin.