alzheimer research

Feb 2006
14,431
2,973
California
Feb 2006
14,431
2,973
California
Out yesterday!

Slow blood vessel pulses could massage away Alzheimer's brain plaques
While plenty of mystery still surrounds how exactly Alzheimer's disease takes hold in the human brain, scientists do have some ideas. A leading suspect is a toxic plaque called amyloid-beta, which new research has found could be better cleared away by harnessing natural oscillations in the blood vessels known as vasomotion.
 
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imaginethat

Forum Staff
Oct 2010
69,521
29,426
Colorado
While I really appreciate the information, Intangible, I must remind EVERYONE that diets, supplements, and easy fixes are not going to reverse dementia. When we read these articles carefully we should immediately recognize them for what they are: possibilities.
Almost every paragraph contains precautionary language such as: Might help. May lead. Might prevent. Possible involvement. Could potentially benefit.

AND here's the danger. Just as with cancer treatment, patients were so desperate for a cure they often LEFT the medical community in search of a possible life-saving drug/herb/voodoo magic. A friend of mine was diagnosed with Guillain-Barré Syndrome. While she was recovering she came across an ad for stem-cell treatments (WHICH WOULD cure her!). She paid $15,000 for the pills. Obviously, she was taken for a ride. This is just one of many examples.

Let's be cautious.
And let's keep in mind that the claim that the damage from Alzheimer's disease or other causes cannot be reversed has beenn and is being challenged.

can brain damage be reversed

Too many drawn to the practice of medicine enjoy the god-like powers associated with it. Pasteur's germ theory was dismissed. Heavier-than-air flight was deemed impossible. Einstein dismissed the idea of humans harnessing nuclear energy.

I am so encouraged that a few brave souls embedded in mainstream medical practice are challenging "what everybody knows" about Alzheimer's and other "hopeless" diseases.

Alzheimer’s disease (AD) is characterized by impairment of hippocampal episodic memory performance followed by a progressive decline of cognitive and social capabilities. Since AD is the major cause of cognitive decline and no curative drug has been developed, research worldwide is intense and highly competitive. Epidemiological, biochemical, molecular, genetic and animal studies provide different entry points into the complex disease process, which led to different theories about the aetiology of AD. Starting with age as the main cause and primary risk factor, AD is being explained by the oligomeric amyloid beta (Aβ) cascade hypothesis, which includes hyperphosphorylated and dysregulated tau [1], the intoxication hypothesis [24], chronic infections [57], microbiome composition [8], neuronal insulin resistance [9, 10], physical and functional breakdown of the blood–brain-barrier (BBB) [11, 12], chronic neuroinflammation, due to multiple causes [13], impaired neuronal rejuvenation (NRJ) [14], synaptic failure [15], and a growing list of many others.​
All of these theories are more or less deeply embedded in the belief that aging per se is the main etiological cause. In fact, the thought that aging per se is the primary cause of AD is so deeply engrained in our thinking and appears in almost every introduction in any scientific paper about AD to be a compulsory statement, which is rarely challenged. But as I will argue, not only are there a number of serious arguments challenging the “age-is-the-primary-cause-dogma”, ageing as the overarching cause also hinders the development of a “unified theory of AD” (UTAD), which incorporates all key findings including the long list of well-known environmental and behavioural risk factors, hence explaining the aetiology and pathogenesis of this debilitating disease. In fact, the lack of a UTAD continues to limit the development of effective preventive measures and a curative treatment to trial and error. Therapeutic interventions that focus on such singled out mechanisms continue to fail [16]. In addition, prevention trials, which rather base their regimen on the correction of more or less arbitrarily selected risk factors than on a complete theory of AD, were so far also limited in their overall success [17, 18]. In contrast, the proposed UTAD overcomes our concept of age per se as the major cause for AD, and provides an encompassing explanation of the aetiology and pathogenesis of Alzheimer’s. It also allows proposing a number of required individual life changing interventions in order to prevent AD with high probability. In addition, the UTAD might provide the logical framework for a curative regimen, as will be outlined at the end of this review.​

You'd probably find the paper quite interesting, Clara.

 
Dec 2015
18,850
18,259
Arizona
And let's keep in mind that the claim that the damage from Alzheimer's disease or other causes cannot be reversed has beenn and is being challenged.

can brain damage be reversed

Too many drawn to the practice of medicine enjoy the god-like powers associated with it. Pasteur's germ theory was dismissed. Heavier-than-air flight was deemed impossible. Einstein dismissed the idea of humans harnessing nuclear energy.

I am so encouraged that a few brave souls embedded in mainstream medical practice are challenging "what everybody knows" about Alzheimer's and other "hopeless" diseases.

Alzheimer’s disease (AD) is characterized by impairment of hippocampal episodic memory performance followed by a progressive decline of cognitive and social capabilities. Since AD is the major cause of cognitive decline and no curative drug has been developed, research worldwide is intense and highly competitive. Epidemiological, biochemical, molecular, genetic and animal studies provide different entry points into the complex disease process, which led to different theories about the aetiology of AD. Starting with age as the main cause and primary risk factor, AD is being explained by the oligomeric amyloid beta (Aβ) cascade hypothesis, which includes hyperphosphorylated and dysregulated tau [1], the intoxication hypothesis [24], chronic infections [57], microbiome composition [8], neuronal insulin resistance [9, 10], physical and functional breakdown of the blood–brain-barrier (BBB) [11, 12], chronic neuroinflammation, due to multiple causes [13], impaired neuronal rejuvenation (NRJ) [14], synaptic failure [15], and a growing list of many others.​
All of these theories are more or less deeply embedded in the belief that aging per se is the main etiological cause. In fact, the thought that aging per se is the primary cause of AD is so deeply engrained in our thinking and appears in almost every introduction in any scientific paper about AD to be a compulsory statement, which is rarely challenged. But as I will argue, not only are there a number of serious arguments challenging the “age-is-the-primary-cause-dogma”, ageing as the overarching cause also hinders the development of a “unified theory of AD” (UTAD), which incorporates all key findings including the long list of well-known environmental and behavioural risk factors, hence explaining the aetiology and pathogenesis of this debilitating disease. In fact, the lack of a UTAD continues to limit the development of effective preventive measures and a curative treatment to trial and error. Therapeutic interventions that focus on such singled out mechanisms continue to fail [16]. In addition, prevention trials, which rather base their regimen on the correction of more or less arbitrarily selected risk factors than on a complete theory of AD, were so far also limited in their overall success [17, 18]. In contrast, the proposed UTAD overcomes our concept of age per se as the major cause for AD, and provides an encompassing explanation of the aetiology and pathogenesis of Alzheimer’s. It also allows proposing a number of required individual life changing interventions in order to prevent AD with high probability. In addition, the UTAD might provide the logical framework for a curative regimen, as will be outlined at the end of this review.​

You'd probably find the paper quite interesting, Clara.

The paper? You mean War and Peace (regarding Alzheimers)?? LOL and=>Yikes, IT. I'm pretty well educated, very well-read (particularly on this subject) and I could barely make it through the first few paragraphs. This lengthy medical harangue was most certainly not written for the lay-person.
I have no doubt that a decade from now the medical community of neuroscientists will be zeroing in on the causes and cures, but that certainly doesn't help the current population of 5.8 million who are living with it. All but 200,000 of these patients are over the age of 65, so to suggest this is NOT a disease deeply encamped in old age is nuts.

I WAS able to translate all the medical jargon into SOME semblance of order but it turns out to be the same ol'
same ol'....like... Diet/nutrition, exercise, healthy living, expanding the mind, using the brain, genetics, human evolution, vitamins (really?), trace elements, body comp and weight, social engagement, sleep deprivation, environmental toxins,
smoking, alcohol, pesticides, and just plain lifestyle.
Risk factors. Of course---why didn't anyone else think of that? Then the final coup de gras:
Furthermore, monotherapeutic treatment strategies that ignore the primary causes and deficiencies should be replaced by a systems-biological approach that is to be initiated as early as possible in the course of disease aiming at eliminating all disease-causing factors in order to give the patient a fighting chance to reverse cognitive decline.
Dr. Michael Nehls


Through some of our personal journey we have been "mentored" by Dr. Marwan Sabbaugh, who I'm certain, would approve of most of Dr. Nehl's findings. Sabbaugh agrees that diet, exercise, and all the rest play a huge part in this age-related disease. He would not agree that the disease can be reversed by following any or ALL the above "remedies". One of the flaws in Dr. Nehls's theories is the "early as possible in the course of the disease".
When is that? When does the disease show itself? When does it surface LONG enough and OFTEN enough to holler ALERT?? I do know the answer to that. For Mr. Clara it was 2 years and by that time the abnormalities were deeply cemented and there's no reversing ANYTHING.
Doctors can stabilize, control the psychological ups and downs, the emotional roller coaster, the weirdness/inappropriate behavior---the crazy part---but it's too late. What Nehl's is asking isn't even possible when you are dealing with people who can't remember ANYTHING, but they are supposed to stick to a strict regimen of diet, exercise, vitamins, social engagement and expanding the mind? Mr. Clara spends DAYS sleeping. He can't remember IF HE ATE or WHAT he ate. He becomes abusive and belligerent if pushed. He has hallucinations. He wanders at night--at all hours, but he needs a sleep regimen? Sorry--I don't mean to take out my frustration on you.

IT, thank you for posting the article. As you can tell from my response, this is a very scary, emotional topic for me. I don't claim to be right or wrong about Dr. Nehl's theories. I don't claim to understand it all. I can only tell you what most of us have lived through and continue to live through---a slithering, viperous killer disease that shows no mercy. Our spouses experience a VERY slow death and we watch it in real-time.
Nancy Reagan was right: It's the long goodbye.