Editorial


A mechanism for ultrasound/light-induced biostimulation

Andrei P. Sommer

Abstract

Alzheimer’s disease was first identified more than 100 years ago, but 70 years passed before it was recognized as the most common cause of dementia and a major killer (1,2). The disease is primarily characterized by a massive decline in memory and cognitive skills, which is caused by neuronal dysfunction and damage, in particular in parts of the brain involved in cognitive function. Although research focusing on the mechanism of Alzheimer’s has progressed a lot, much is yet to be done to prevent, delay or stop the disease. Expectations to ameliorate the disease are mostly fuelled by the pharmaceutical side. Virtually all of the 1.000.000 Google hits found for the key words breakthrough and Alzheimer’s are related to some new drug. In view of this overwhelming trend, nobody expected the possibility of a potential solution from the physical side. Therefore, the recently reported substantial reduction of Aβ42 plaques in the brain of mice by the synergistic interplay of transcranially applied ultrasound waves and biologically inert micron sized microbubbles has a strong momentum of surprise (3). Leinenga and Götz report on two apparently (?) independent phenomena: the transient opening of the blood brain barrier (BBB) by ultrasound induced modulation (expansion and contraction) of the microbubbles (acoustic cavitation), and importantly, a concomitant reduction of the Aβ42 plaques in the brain of the test animals. These results were achieved in two subsequent steps: intravenous injection of microbubbles, and transcranial application of low levels of focused ultrasound waves with a pulse repetition frequency of 10 Hz. The duration of the treatment was 6 weeks—a promising scenario. Reportedly, the clearance of the Aβ42 deposits involved phagocytosis by microglia with uptake into lysosomes.

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