Posted: Oct 30, 2016 4:10 pm
by Calilasseia
The world of Alzheimer's disease research is littered with failures, not to mention undue hype for those failures before they're found to fail, and more than its fair share of quackery. But a team of scientists, working at the University of Queensland (specifically, the Queensland Brain Institute) have alighted upon a therapeutic procedure that, for once, looks as if it's going to deliver some success.

Courtesy of this paper in Science Translational Medicine, we learn that scanning ultrasound has been demonstrated to be successful in removing β-amyloid plaques from the brain, at least in the mouse model. The scientists in question are hoping to move on to higher models, and begin preliminary human trials sometime in 2017.

The reason this treatment is attracting attention, is because it doesn't involve drugs, and is, like foetal ultrasound scanning, effectively non-invasive. If this works as well in humans as it does in the mouse model, then we could be on the verge of a significant move forward in our understanding of this condition.


The paper in question is:

Scanning Ultrasound Removes Amyloid-β And Restores Memory In An Alzheimer’s Disease Mouse Model by Gerhard Leinenga and Jürgen Götz, Science Translational Medicine, 7: 288-321 (11th March 2015) DOI: 10.1126/scitranslmed.aaa2512

Leinenga & Götz, 2015 wrote:Abstract

Amyloid-β (Aβ) peptide has been implicated in the pathogenesis of Alzheimer’s disease (AD). We present a nonpharmacological approach for removing Aβ and restoring memory function in a mouse model of AD in which Aβ is deposited in the brain. We used repeated scanning ultrasound (SUS) treatments of the mouse brain to remove Aβ, without the need for any additional therapeutic agent such as anti-Aβ antibody. Spinning disk confocal microscopy and high-resolution three-dimensional reconstruction revealed extensive internalization of Aβ into the lysosomes of activated microglia in mouse brains subjected to SUS, with no concomitant increase observed in the number of microglia. Plaque burden was reduced in SUS-treated AD mice compared to sham-treated animals, and cleared plaques were observed in 75% of SUS-treated mice. Treated AD mice also displayed improved performance on three memory tasks: the Y-maze, the novel object recognition test, and the active place avoidance task. Our findings suggest that repeated SUS is useful for removing Aβ in the mouse brain without causing overt damage, and should be explored further as a noninvasive method with therapeutic potential in AD.