Summary: Scanning ultrasound appears to slow down aging in healthy brains, a new study reports.
Source: University of Queensland.
Treatment with scanning ultrasound has already been proven to reverse Alzheimer’s disease in mice, and now it appears it could also slow down ageing in healthy brains, according to University of Queensland research.
The research is the latest work from Professor Jürgen Götz’s lab in the Clem Jones Centre for Ageing Dementia Research at the Queensland Brain Institute.
It showed that scanning ultrasound prevented degeneration of cells in the brains of healthy mice.
Researcher Dr Robert Hatch said the work was originally designed as a safety study, but soon revealed a broader role for ultrasound in maintaining brain health.
“We found that, far from causing any damage to the healthy brain, ultrasound treatments may in fact have potential beneficial effects for healthy ageing brains,” Dr Hatch said.
“In a normal brain the structure of neuronal cells in the hippocampus, a brain area extremely important for learning and memory, is reduced with age.
“What we found is that treating mice with scanning ultrasound prevents this reduction in structure, which suggests that by using this approach we can keep the structure of the brain younger as we get older.
“We are currently conducting experiments to see if this preservation of the brain cell structure will ameliorate reductions in learning and memory that occur with ageing.”
The mice were treated with either one or six scanning ultrasound treatments over six weeks. Their brain cell structure and function were reviewed two hours, one day, one week, and three months after receiving the treatment.
In the next stage of research, the team will test the effect of ultrasound on the brain structure and function of older mice.
Professor Götz’s lab has previously shown that non-invasive ultrasound technology can reverse Alzheimer’s disease in mice.
The approach is able to temporarily open the blood-brain barrier, activating mechanisms that clear toxic protein clumps and restore memory functions.
“Collectively, this research is fundamentally changing our understanding of not only how to treat Alzheimer’s but to maintain general brain health,” Dr Hatch said.
“This is a pressing health issue in an ageing society and it’s clear that scanning ultrasound technology has a major role to play.”
Alzheimer’s affects more than two thirds of dementia patients, and about a quarter of a million Australians.
The total number of dementia cases in Australia is expected to rise to 900,000 by 2050.
Funding: The research, published in PloS One, was funded by the estate of Dr Clem Jones and by grants from the Australian Research Council (ARC), the National Health and Medical Research Council, and the ARC Linkage Infrastructure, Equipment and Facilities scheme.
Source: Kirsten MacGregor – University of Queensland
Image Source: NeuroscienceNews.com image is credited to Hatch et al./PLOS ONE.
Original Research: Full open access research for “Scanning Ultrasound (SUS) Causes No Changes to Neuronal Excitability and Prevents Age-Related Reductions in Hippocampal CA1 Dendritic Structure in Wild-Type Mice” by Robert John Hatch, Gerhard Leinenga, and Jürgen Götz in PLOS ONE. Published online October 11 2016 doi:10.1371/journal.pone.0164278
Scanning Ultrasound (SUS) Causes No Changes to Neuronal Excitability and Prevents Age-Related Reductions in Hippocampal CA1 Dendritic Structure in Wild-Type Mice
Scanning ultrasound (SUS) is a noninvasive approach that has recently been shown to ameliorate histopathological changes and restore memory functions in an Alzheimer’s disease mouse model. Although no overt neuronal damage was reported, the short- and long-term effects of SUS on neuronal excitability and dendritic tree morphology had not been investigated. To address this, we performed patch-clamp recordings from hippocampal CA1 pyramidal neurons in wild-type mice 2 and 24 hours after a single SUS treatment, and one week and 3 months after six weekly SUS treatments, including sham treatments as controls. In both treatment regimes, no changes in CA1 neuronal excitability were observed in SUS-treated neurons when compared to sham-treated neurons at any time-point. For the multiple treatment groups, we also determined the dendritic morphology and spine densities of the neurons from which we had recorded. The apical trees of sham-treated neurons were reduced at the 3 month time-point when compared to one week; however, surprisingly, no longitudinal change was detected in the apical dendritic trees of SUS-treated neurons. In contrast, the length and complexity of the basal dendritic trees were not affected by SUS treatment at either time-point. The apical dendritic spine densities were reduced, independent of the treatment group, at 3 months compared to one week. Collectively, these data suggest that ultrasound can be employed to prevent an age-associated loss of dendritic structure without impairing neuronal excitability.
“Scanning Ultrasound (SUS) Causes No Changes to Neuronal Excitability and Prevents Age-Related Reductions in Hippocampal CA1 Dendritic Structure in Wild-Type Mice” by Robert John Hatch, Gerhard Leinenga, and Jürgen Götz in PLOS ONE. Published online October 11 2016 doi:10.1371/journal.pone.0164278