Will Alzheimer Sufferers Start Attending Raves?

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Will Alzheimer Sufferers Start Attending Raves?

Postby BadgerJelly on March 14th, 2019, 12:48 pm 

Flickers and buzzes sweep mouse brains of Alzheimer’s plaques


Fast clicking sounds can boost brainpower in mice with signs of Alzheimer’s disease. Like flickering lights, these external sounds spur a type of brain wave that seemed to sweep disease-related plaques from mice’s brains, researchers report in the March 14 Cell.

It’s too early to say whether the same sorts of flickers and clicks could help people with Alzheimer’s. If so, the treatment would represent a fundamentally new way to target the neurodegenerative disease — with lights and sounds instead of drugs.

Effects on humans?:

It’s also not known whether the results in these genetically engineered mice, which mimic a rare and aggressive form of Alzheimer’s, would apply to people. Tsai has cofounded a company, Cognito Therapeutics, that is testing the combined light-and-sound approach in older people with mild to moderate cognitive impairment. The study isn’t done yet, Tsai says, but so far “we haven’t seen any undesirable effects.”
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Re: Will Alzheimer Sufferers Start Attending Raves?

Postby doogles on March 15th, 2019, 4:26 am 

We had a thread going the other day about red flags to quackery in medicine. There was some discussion about evidence-based medicine sometimes being questionable, and that Pharma-medicine may sometimes be stretching 'evidence' just a bit far. Alzheimers Disease (AD) research is probably exemplary of the amount of time and energy being put into the esoteric studies of a condition in an attempt to find a cure or preventative. The financial rewards to a pharmaceutical company would be large. I think we would all pop a pill a day if we thought it would stabilise our mental integrity.

I looked at Google Scholar, only to discover that scores of research papers on AD have already been published this year alone (2019). If anyone was doing a PhD thesis on the subject, I believe the maximum 400 pages would be taken up by the critical literature-review alone. Almost all deal with esoteric investigations into tau, amyloid, alpha-synuclein, TDP-43 and apolipoproein E involvement in dementias.

I liked Badger's sense of humour in his title to this thread, but the experiment he cited is just another esoteric investigation. Whether dissolving beta-amyloids with sound or light flickering will produce any benefits remains to be seen. One of the 2019 papers on this site -- https://www.biorxiv.org/content/10.1101 ... 1.abstract) records that Pulina et al (2019) developed a sensitive assay for the detection of C99, an intermediate in the conversion of APP to beta-amyloid. Brain tissue sections were obtained from patients suffering from sporadic AD and non-demented controls. Their results demonstrate that "C99 levels, but NOT Abeta levels, correlate with the degree of vulnerability to neurodegeneration and cognitive impairment in patients suffering from AD."

Of course, there is a possibility that the flickering light and sound therapy may do more than just dissolve beta-amyloid proteins.

What concerns me about all of this Alzheimers' Disease research is that those involved appear to be minutely dissecting trees instead of looking at the forest as a whole. I don't understand why researchers have not picked up on the following papers:
Allison (2001; https://www.sciencedirect.com/science/a ... 7701913076) offered a theory associating vitamin K deficiency with Alzheimer's Disease. The hypothesis was that vitamin K deficiency contributes to the pathogenesis of Alzheimer's Disease and that vitamin K supplementation may have a beneficial effect in preventing or treating the disease. Vitamin K may also reduce neuronal damage associated with cardiovascular disease.
Presse et al (2008; http://www.ncbi.nlm.nih.gov/pubmed/1902 ... t=Abstract) assessed the amount of vitamin K in the diets on 5 non-consecutive days in 31 community-dwelling patients with early Alzheimer's Disease and compared 31 age and sex-matched controls without the disease. They found a highly significant association between low mean vitamin K intake and Alzheimer's Disease, the mean intake of the first and second groups being 63 and 139 micrograms per day respectively. I have a reservation about the statistical result in this study though because the respective variations about the mean values were listed in the abstract as +/- 90 and 233 micrograms respectively.
Ferland (2012; https://academic.oup.com/advances/artic ... 04/4557944) summarised the role of vitamin K in nervous system health. He pointed out that the role of vitamin K in nervous system function has been somewhat neglected in spite of the fact that it was identified as being essential for the synthesis of sphingolipids since about the 1980s. He added that these sphingolipids are now known to be vitally involved in the structure of the nervous system, and possess cell signalling functions as well. Amongst the many roles that vitamin K-dependent proteins play throughout the nervous system, Protein Gas6 (Growth arrest-specific protein, which has much in common with Protein S (A vitamin K-dependent anticoagulent protein) has been shown to be vitally involved in cell survival, chemotaxis, mitogenesis, and cell growth of neurons and glial cells. The author points out that a limited amount of literature suggests that vitamin K is also involved in behaviour and cognition.

Vitamin K also reverses atherosclerosis, and atherosclerosis has been shown to be a common factor in dementia -- Hofmann et al (1997; https://www.sciencedirect.com/science/a ... 3696093282) found, in a study of 284 patients with dementia, 207 of whom had Alzheimer's disease, that all indicators of atherosclerosis were associated with dementia (odds ratios ranging from 1·3 to 1·9) and its major subtypes Alzheimer's disease (odds ratios 1·3–1·8) and vascular dementia (odds ratios 1·9–3·2). The frequencies of all dementia, Alzheimer's disease, and vascular dementia increased with the degree of atherosclerosis. The odds ratio for Alzheimer's disease in those with severe atherosclerosis compared with those without atherosclerosis was 3·0 (95% CI 1·5–6·0; P=0·001).
Hughes et al (2018; http://n.neurology.org/content/90/14/e1248) measured Pulse Wave Velocities of carotid-femoral and heart-carotid segments to obtain measurements of the general 'stiffness' of arteries (arteriosclerosis - my comment). They compared these with scores for Dementia and Moderate Cognitive Impairment. Greater carotid-femoral stiffness was significantly associated with lower brain volumes in Alzheimer's and high white matter intensity burden. The associations were strongest in cases of Mild Cognitive Impairment.

Why haven't these investigations been followed up? It would only require about 4 groups of 10 subjects in a retirement village using adequate vitamin K in the treatment groups for a few months to get a positive result. The vitamin is cheap and one of the safest substances on the planet. There are NO recorded side effects. The largest cost would be for a postgraduate student to do the cognitive scoring tests, and for the clerical work involved in organising the project.
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