Alzheimer’s treatment fully restores memory function (2015) (opens in new tab)

And it doesn't have to be - the side effects are to be weighted against the benefits.

however it has been proven that Alzheimer's is completely unsafe for the brain.

Both my grandmothers. It's brutal - from what we can tell in retrospect both of them were probably very aware of it, possibly for 2-3 years, but terrified of admitting to it.

One had a breakdown when her husband was going into hospital for a minor operation and she was terrified she wouldn't be able to take care of herself. The other had to be tricked to come in for an evaluation because she was scared of being left at the hospital.

Both lived for years after they stopped recognising anyone or reacting to stimuli, and the worst part to me was that both my grandfathers ended up spending years putting their own last years on hold to care for someone who no longer showed any signs of remembering who they were.

For all intents and purposes they were gone, but because they were still physically alive, it locked people in this waiting pattern. One of my grandfathers pretty much spent all his waking hours sitting next to his wife in a nursing home from he turned 80 until ca. 90. When she finally died, he was able to do other things again, but then died two years later of heart failure (he'd had heart problems since his 50s)

Have to start somewhere. This is a big deal for a number of reasons. This provides a non-invasive treatment avenue for a very common (35M worldwide and expected to double in 20 years) CNS affliction and shows incredible curative properties in animal models.

This is real science.

Briefly, the authors repeatedly, transiently opened the blood-brain barrier (BBB) of an animal model of AD using scanning ultrasound. They observed that AD-like behavioral and brain symptomology was reduced in the treated animals. They suggest that the effects may be related to potentiating bloodflow to the brain and thereby enhancing clean-up of AD-related pathology.

The challenges going forward are described in their limitations section:

"At this stage, several hurdles have to be faced for SUS to be considered for application in human patients. In addition to the limitation presented by the animal model used in our study, it needs to be considered that the human brain is much larger than that of a mouse. Also, the thicker human skull presents an obstacle that needs to be factored in when parameters are defined that have the envisaged biological effect in the absence of tissue damage. There may also be the necessity to use one of several cranial windows to access the human brain. Also, if one were to apply SUS in humans at the prodromal stage before overt symptoms of AD were present, the safety of this approach would need to be monitored in real time. This could be facilitated by the recent development of advanced methods, such as passive cavitation detection, which is currently being evaluated in both rodents and primates (29). To avoid potentially excessive immune activation in a clinical setting (30), the ultrasound treatment regimen could possibly be done stepwise, covering one brain area at a time.Whereas we only coupled ultrasound with microbubbles, previous studies in rodents evaluated ultrasound for the delivery of therapeutic agents, such as antibodies (31, 32), viral vectors (33), and dextran of different sizes (9, 10). One study targeted Ab using a few entry points for delivery and only a single treatment (34). Because the effect on Ab plaques was very modest, the authors of this study suggested that focused ultrasound would best be suited as a delivery tool, for example, to boost the uptake of peripherally administered anti-Ab antibodies (34). Our results, however, demonstrated that repeated SUS treatment of the entire mouse brain was sufficient to markedly ameliorate the pathology of Ab-depositing mice as analyzed histologically, biochemically, and behaviorally.Our study highlights the potential of SUS treatment as a therapeutic approach for AD and possibly other diseases involving protein aggregation. However, this does not rule out the possibility that it could also be used as a vehicle for drug or gene delivery, given that the BBB remains themajor obstacle for the uptake by brain tissue of therapeutic agents from the circulation (9)."

In summary, it's an interesting approach, but I'm not holding my breath.

And "in mice"?