[Tanada]

New Alzheimer’s Treatment Fully Restores Memory Function

Australian researchers have come up with a non-invasive ultrasound technology that clears the brain of neurotoxic amyloid plaques - structures that are responsible for memory loss and a decline in cognitive function in Alzheimer’s patients.

If a person has Alzheimer’s disease, it’s usually the result of a build-up of two types of lesions - amyloid plaques, and neurofibrillary tangles. Amyloid plaques sit between the neurons and end up as dense clusters of beta-amyloid molecules, a sticky type of protein that clumps together and forms plaques.

Neurofibrillary tangles are found inside the neurons of the brain, and they’re caused by defective tau proteins that clump up into a thick, insoluble mass. This causes tiny filaments called microtubules to get all twisted, which disrupts the transportation of essential materials such as nutrients and organelles along them, just like when you twist up the vacuum cleaner tube.

As we don’t have any kind of vaccine or preventative measure for Alzheimer’s - a disease that affects 343,000 people in Australia, and 50 million worldwide - it’s been a race to figure out how best to treat it, starting with how to clear the build-up of defective beta-amyloid and tau proteins from a patient’s brain. Now a team from the Queensland Brain Institute (QBI) at the University of Queensland have come up with a pretty promising solution for removing the former.

Publishing in Science Translational Medicine, the team describes the technique as using a particular type of ultrasound called a focused therapeutic ultrasound, which non-invasively beams sound waves into the brain tissue. By oscillating super-fast, these sound waves are able to gently open up the blood-brain barrier, which is a layer that protects the brain against bacteria, and stimulate the brain’s microglial cells to activate. Microglial cells are basically waste-removal cells, so they’re able to clear out the toxic beta-amyloid clumps that are responsible for the worst symptoms of Alzheimer’s.

The team reports fully restoring the memory function of 75 percent of the mice they tested it on, with zero damage to the surrounding brain tissue. They found that the treated mice displayed improved performance in three memory tasks - a maze, a test to get them to recognise new objects, and one to get them to remember the places they should avoid.

"We’re extremely excited by this innovation of treating Alzheimer’s without using drug therapeutics," one of the team, Jürgen Götz, said in a press release. "The word ‘breakthrough’ is often misused, but in this case I think this really does fundamentally change our understanding of how to treat this disease, and I foresee a great future for this approach."

The team says they’re planning on starting trials with higher animal models, such as sheep, and hope to get their human trials underway in 2017.

http://www.sciencealert.com/new-alzheim ... y-function

[Cog]

Thanks Tanada for posting this. Sounds like an interesting non-chemical approach to a very big problem facing the baby-boomers like myself.

[sparky]

.
https://www.sciencedaily.com/releases/2 ... 160635.htm
a good way of keeping your brain in good shape is smoking , of course , your lungs will take a hit but that's life
it give and it take , there is a price for everything .
drinking a bottle of red wine a day is good for your blood flow but your liver will bear the cost

I've been smoking for a very long while now and everything is fine ,
someone in the family got Alzheimer but I can't remember whom

[careinke]

.
https://www.sciencedaily.com/releases/2 ... 160635.htm
a good way of keeping your brain in good shape is smoking , of course , your lungs will take a hit but that's life
it give and it take , there is a price for everything .
drinking a bottle of red wine a day is good for your blood flow but your liver will bear the cost

I've been smoking for a very long while now and everything is fine ,
someone in the family got Alzheimer but I can't remember whom

My mother was an avid cigarette smoker. Right up till the day she forgot she smoked. Didn't seem to stop her Alzheimers......

I'm trying exercising while stoned on pot. Supposed to break down the Blood brain barrier, and flush out the plaque. It may not work, but worth the try. LOL

[dissident]

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2769828/

Alzheimer's disease (AD) has characteristic histopathological, molecular, and biochemical abnormalities, including cell loss; abundant neurofibrillary tangles; dystrophic neurites; amyloid precursor protein, amyloid-β (APP-Aβ) deposits; increased activation of prodeath genes and signaling pathways; impaired energy metabolism; mitochondrial dysfunction; chronic oxidative stress; and DNA damage. Gaining a better understanding of AD pathogenesis will require a framework that mechanistically interlinks all these phenomena. Currently, there is a rapid growth in the literature pointing toward insulin deficiency and insulin resistance as mediators of AD-type neurodegeneration, but this surge of new information is riddled with conflicting and unresolved concepts regarding the potential contributions of type 2 diabetes mellitus (T2DM), metabolic syndrome, and obesity to AD pathogenesis. Herein, we review the evidence that (1) T2DM causes brain insulin resistance, oxidative stress, and cognitive impairment, but its aggregate effects fall far short of mimicking AD; (2) extensive disturbances in brain insulin and insulin-like growth factor (IGF) signaling mechanisms represent early and progressive abnormalities and could account for the majority of molecular, biochemical, and histopathological lesions in AD; (3) experimental brain diabetes produced by intracerebral administration of streptozotocin shares many features with AD, including cognitive impairment and disturbances in acetylcholine homeostasis; and (4) experimental brain diabetes is treatable with insulin sensitizer agents, i.e., drugs currently used to treat T2DM. We conclude that the term “type 3 diabetes” accurately reflects the fact that AD represents a form of diabetes that selectively involves the brain and has molecular and biochemical features that overlap with both type 1 diabetes mellitus and T2DM.

The ultrasound treatment is wonderful. But there is a dietary and genetic predisposition component to Alzheimer's as well.

[careinke]

Hi All,

I recently took a 23 and me genetic test. It not only checked for ancestry, it also checked for health traits. Unfortunately, I picked up traits for late onset Alzheimer's from both mom and dad. This significantly increases my risk of getting late onset Alzheimer's myself. Although I'm not happy with it, it is what it is.

A quick review of current standard medical practices, show that they have not made any advances since my mom died. Basically, there is no cure or prevention for Alzheimer’s. That said, there are some promising approaches I will be pursuing which may help. These include a keto diet, intermittent fasting, exercise, and some brain training exercises.

I figure these approaches will be beneficial to me even if I don't end up with Alzheimer's.

I'm not looking for sympathy here, but figured some of you may want to keep up with my progress, for future reference. I plan to stay with the board, because you guys always provide lots to think about.

If I do contract the disease, I apologize in advance for all the horrible things I will call you or blame you for.

[dissident]

There is no cure is not really the issue. There is clearly an insulin link which can be controlled by diet and exercise. As an added bonus the rest of the metabological syndrome (which includes heart disease) can be controlled as well.

The key detail is not to follow the joke called the food pyramid and the advice of any of the "Associations" as to what you should eat. Everyone has to tailor their diet to their own metabolism. This is difficult to do and requires long term commitment which for humans is a real challenge.

[Tanada]

Below is the abstract of a 5.3 Mb report on using common X-ray machines as a treatment for Alzheimer's Disease. Unfortunately because the treatment is a) very inexpensive and b) has no copy-written new pharmacological component the FDA has expressed very little interest in it. Two years ago I posted an article about a similar treatment that prevented the Cytokine "storm" in patients with Covid-19 which had the same problem, nobody was going to get rich selling that treatment so it was passed over in favor of multiple inoculation treatments where the vaccine company get repeated payments from Federal funds for every inoculation. The first link is direct to the publication page for the report, the second is to the PDF of the report in case you want to save your own copy for reading slowly as it is very long and detailed.

Neuroprotective and Anti-Inflammatory Effects of Low–Moderate Dose Ionizing Radiation in Models of Alzheimer’s Disease

Alzheimer’s disease (AD) is the most common cause of dementia. The neuropathological features of AD include amyloid-β (Aβ) deposition and hyperphosphorylated tau accumulation. Although several clinical trials have been conducted to identify a cure for AD, no effective drug or treatment has been identified thus far. Recently, the potential use of non-pharmacological interventions to prevent or treat AD has gained attention. Low-dose ionizing radiation (LDIR) is a non-pharmacological intervention which is currently being evaluated in clinical trials for AD patients. However, the mechanisms underlying the therapeutic effects of LDIR therapy have not yet been established. In this study, we examined the effect of LDIR on Aβ accumulation and Aβ-mediated pathology. To investigate the short-term effects of low–moderate dose ionizing radiation (LMDIR), a total of 9 Gy (1.8 Gy per fraction for five times) were radiated to 4-month-old 5XFAD mice, an Aβ-overexpressing transgenic mouse model of AD, and then sacrificed at 4 days after last exposure to LMDIR. Comparing sham-exposed and LMDIR-exposed 5XFAD mice indicated that short-term exposure to LMDIR did not affect Aβ accumulation in the brain, but significantly ameliorated synaptic degeneration, neuronal loss, and neuroinflammation in the hippocampal formation and cerebral cortex. In addition, a direct neuroprotective effect was confirmed in SH-SY5Y neuronal cells treated with Aβ1–42 (2 μM) after single irradiation (1 Gy). In BV-2 microglial cells exposed to Aβ and/or LMDIR, LMDIR therapy significantly inhibited the production of pro-inflammatory molecules and activation of the nuclear factor-kappa B (NF-κB) pathway. These results indicate that LMDIR directly ameliorated neurodegeneration and neuroinflammation in vivo and in vitro. Collectively, our findings suggest that the therapeutic benefits of LMDIR in AD may be mediated by its neuroprotective and anti-inflammatory effects.
Keywords: Alzheimer’s disease, low-moderate dose ionizing radiation, radiotherapy, 5XFAD mice, neurodegeneration, neuroinflammation

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