Research pioneered at Monash University has potentially discovered an effective new treatment for dementia, specifically for a rare form of the disease called behavioural variant frontotemporal dementia (bvFTD).
Behavioural variant frontotemporal dementia is the second most prominent form of the disease in people under 60 and causes stabilisation of what would traditionally be increasing behavioural issues in dementia patients and a slowing of the brain shrinkage typical in the condition.
A clinical trial performed at Monash University may offer a novel treatment for dementia, finding that the drug sodium selenate can mitigate cognitive decline and neurodegenerative damage that characterise a plethora of dementias, including Alzheimer’s disease.
The research, which Dr Lucy Vivash led from the Monash University’s Department of Neuroscience, is published in the journal Alzheimer’s and Dementia: Translational Research and Clinical Interventions.
Impacts of bvFTD
Behavioural variant frontotemporal dementia is a form of neurodegenerative disease that progresses rapidly and can affect people as young as 35. The condition causes behavioural and personality changes that can be incredibly disruptive and disturbing for patients and families. Most people die from the disease within five to seven years of their diagnosis. Unfortunately, there are currently no effective treatments or cures for bvFTD, meaning this novel treatment for dementia could change the lives of thousands of people globally.
Innovating a new treatment for dementia
The team’s Phase 1 trial was performed in collaboration with researchers at The Royal Melbourne Hospital, which is the only hospital in Australia and one of the few worldwide targeting non-genetic bvFTD. The study signified that the sodium selenate treatment for dementia was well-tolerated and safe in patients over a period of 12 months.
Most notably, the majority of patients that received sodium selenate demonstrated no change in their cognitive or behavioural symptoms and showed reduced rates of brain atrophy during the trial. In around 50% of bvFTD, damage to neurons in the brain is caused by the build-up of a protein called tau.
This accumulation of tau is a major target for preventing and treating dementia and Alzheimer’s disease, as it may be able to reduce neurodegeneration. The researchers explained that sodium selenate upregulates a brain enzyme that breaks down the tau protein.
Dr Vivash concluded: “We have previously shown, in a Phase 2 trial, that sodium selenate given to patients with mild to moderate Alzheimer’s Disease resulted in less neurodegeneration than in those who did not.”
Importantly patients in the trial with higher levels of selenium, a breakdown product of sodium selenate, in their bloodstream displayed lower levels of cognitive decline. The team is now carrying out a more extensive study throughout Australia and New Zealand to investigate further the effects of the drug in patients with bvFTD.