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What is your wavelength?
Lane Simonian
Posted: Thursday, March 26, 2015 10:31 AM
Joined: 12/12/2011
Posts: 4986

There have been a number of small studies regarding the effects of different wavelengths on the onset and progression of Alzheimer's disease. Some of the results were positive, some negative, and some contradictory (for cell phones, for instance). The results differed based not only on the frequency of the wavelength, but the length of exposure, the mode of delivery (continuous or pulsed), and the age at which it was delivered. In general, though, wavelengths that increased inducible nitric oxide synthase are bad for the brain, and those that decrease inducible nitric oxide synthase are good for the brain. Keeping that in mind, here is a somewhat shaky and incomplete list.

Bad for the brain (with prolonged exposure)

Electromagnetic fields (such as high voltage power lines)
Cell phones
Ultrasounds (in spite of the positive results from one mouse study)

Good for the brain

Deep brain stimulation
Cranial helmets
Low Level Laser Therapy (in most cases probably)
Charcoal Bamboo
Near infrared sauna

Some of these treatments are more invasive than others and the idea of potentially altering the electrical system of the brain makes me a bit squeamish. One is better off most likely by sniffing essential oils and taking herbs that both inhibit inducible nitric oxide synthase and scavenge peroxynitrites.

Posted: Tuesday, March 31, 2015 5:18 PM
Joined: 9/13/2013
Posts: 112

I agree that emfs, cell phones can be bad. Many researches have supported this.

But for ultrasound which is used in the medical field a lot, can you please elaborate why it can be bad for the brain?

Lane Simonian
Posted: Tuesday, March 31, 2015 8:05 PM
Joined: 12/12/2011
Posts: 4986

Part of the difficulty in these studies is that certain pathways are beneficial in the relative absence of oxidative stress but can become negative in the presence of oxidative stress. In the case of some of these different wavelengths at least, the activation of the AMP-activated protein kinase with low levels of oxidative stress leads to the activation of the phosphatidyinositol-3 kinase. In the brain, this kinase (via Akt) leads to better blood flow in the brain, upgraded antioxidant defenses, and to neurogenesis. This is the key enzyme that becomes blocked in Alzheimer's disease and when it does the AMP-activated protein kinase leads to the production of inducible nitric oxide instead and inducible nitric oxide combines with superoxide anions to produce peroxynitrites which kill neurons.

So it is not only the wavelength used but when it is applied or put another way what might help people without Alzheimer's disease may not help people with Alzheimer's disease. Or in the mouse world what may be good for young mice may not be good for old mice.

Here is the specific case for (or against) ultrasound treatment:

AMP-activated protein kinase is involved in COX-2 expression in response to ultrasound in cultured osteoblasts.

2015;43(3):775-84. doi: 10.3233/JAD-140564.

AMPK activation ameliorates Alzheimer's disease-like pathology and spatial memory impairment in a streptozotocin-induced Alzheimer's disease model in rats.

2011 Aug;118(4):460-74. doi: 10.1111/j.1471-4159.2011.07331.x. Epub 2011 Jun 24.

AMP-activated protein kinase: a potential player in Alzheimer's disease.

AMP-activated protein kinase (AMPK) stimulates energy production via glucose and lipid metabolism, whereas it inhibits energy consuming functions, such as protein and cholesterol synthesis. Increased cytoplasmic AMP and Ca(2+) levels are the major activators of neuronal AMPK signaling. Interestingly, Alzheimer's disease (AD) is associated with several abnormalities in neuronal energy metabolism, for example, decline in glucose uptake, mitochondrial dysfunctions and defects in cholesterol metabolism, and in addition, with problems in maintaining Ca(2+) homeostasis. Epidemiological studies have also revealed that many metabolic and cardiovascular diseases are risk factors for cognitive impairment and sporadic AD. Emerging studies indicate that AMPK signaling can regulate tau protein phosphorylation and amyloidogenesis, the major hallmarks of AD. AMPK is also a potent activator of autophagic degradation which seems to be suppressed in AD. All these observations imply that AMPK is involved in the pathogenesis of AD. However, the responses of AMPK activation are dependent on stimulation and the extent of activating stress. Evidently, AMPK signaling can repress and delay the appearance of AD pathology but later on, with increasing neuronal stress, it can trigger detrimental effects that augment AD pathogenesis. We will outline the potential role of AMPK function in respect to various aspects affecting AD pathogenesis.

Two questions for which I have no answers: in 75% of the mice with an Alzheimer's-like disease, the ultrasound completely restored memory. What happened in the other 25% of the mice and why? And why does the use of ultrasound to activate the AMP-activated protein kinase lead to spatial memory improvements in mice but likely worsen the progression of Alzheimer's disease in human beings? Is there something different in levels of oxidative stress in mice bred to have an Alzheimer's-like disease versus the level of oxidative stress that triggers Alzheimer's disease in human beings.

I may have just stumbled across the answer, peroxynitrites do not appear to centrally mediate tyrosine nitration in mice, but they do in human beings. It is tryosine nitration mediated primarily by peroxynitrites that cuts off the neuroprotective phosphatidylinositol-3 kinase/Akt pathway in human beings--maybe that is why mice don't get real Alzheimer's disease and and one of the reasons why so many things seem to work in "mouse Alzheimer's disease" but not in human Alzheimer's disease.