Scientists find first drug that appears to slow Alzheimer's disease

[umbertino]

Solanezumab blocks memory loss in patients with mild version of the disease, making it the first medicine ever to slow pace of damage to patients’ brains

 

 

Hannah Devlin Science correspondent

 

Wednesday 22 July 2015 12.15 BST

 

 

 

Scientists appear to have broken a decades-long deadlock in the battle against Alzheimer’s disease after announcing trial results for the first drug that appears to slow the pace of mental decline.

 

The drug, called solanezumab, was shown to stave off memory loss in patients with mild Alzheimer’s over the course of several years. The effects would have been barely discernible to patients or their families, scientists said, and it is no cure. But the wider implications of the results have been hailed as “hugely significant” because it is the first time any medicine has slowed the rate at which the disease damages the brain.

 

“This is the first evidence of something genuinely modifying the disease process,” said Dr Eric Karran, director of research at Alzheimer’s Research UK. “It’s a breakthrough in my mind. The history of medicine suggests that once you get through that door you can explore further therapeutic opportunities much more aggressively. It makes us less helpless.”

 

Existing drugs help with the symptoms but ultimately do nothing to slow the disease’s progression.

 

The drug, developed by the American company Eli Lilly, had previously been tested in a larger group of patients with both mild and moderate dementia and this trial had appeared to end in failure in 2012.

 

However, when scientists analysed the data more closely, they found that in the 1,300 patients with mild dementia, those who had been placed on the drug showed a roughly 30% slower decline in memory and cognitive tests than those who had taken a placebo during the 18-month trial.

 

This was a fairly small difference from the perspective of the patients who had not yet suffered the devastating memory loss or profound changes to personality that come later on. But the result hinted that the drug could work as long as it was given early enough.

 

Questions remained about whether the drug was simply treating the symptoms – improving a patient’s mood or concentration – rather than actually delaying the loss of neurons in the brain, which drives memory loss.

 

To test this, Eli Lilly switched the half of the 1,300 patients who had been on the placebo on to the drug as well and the entire group was given solanezumab for a further two years.

 

If the drug was just treating the symptoms, the placebo group would be expected to “catch up” over time. However, the results, unveiled on Wednesday at the Alzheimer’s Association International Conference in Washington DC, in the US, showed that the differences between the two groups were still there – a sign that the drug had made a genuine impact on the progression of the disease.

 

“It deflected the course of the disease in an irrevocable manner,” said Karran, who previously worked for Eli Lilly.

 

The company is now looking to see whether the drug is more effective when given at an earlier stage – something that might be expected given that it apparently had no effect for patients with more serious dementia. “It’s entirely possible you’ll show an even bigger benefit if people are given solanezumab earlier on,” said Karran.

 

Scientists said the results also support the idea that sticky plaques in the brain – the most visible hallmark of the disease – are what causes mental decline. The drug is an antibody that works by disassembling the building blocks that make up the plaques, slowly causing them to disintegrate.

 

Until now, drugs that targeted the plaques have not appeared to have any effect leading some to question whether some other biological process in Alzheimer’s was the real root of the disease.

 

Dr Doug Brown, head of research at the Alzheimer’s Society, said: “Today’s findings strongly suggest that targeting people in the earliest stages of Alzheimer’s disease with these antibody treatments is the best way to slow or stop Alzheimer’s disease. These drugs are able to reduce the sticky plaques of amyloid that build up in the brain, and now we have seen the first hints that doing this early enough may slow disease progression.”

 

The positive trial results follow years of failed clinical research. Between 2002 and 2012, 99.6% of drugs studies aimed at preventing, curing or improving Alzheimer’s symptoms were either halted or discontinued at huge financial cost to drugs companies, many of whom shut down dementia programmes as a result.

 

Richard Morris, professor of neuroscience at the University of Edinburgh, said the result was likely to be significant – although he added that he was reserving final judgment until he saw the data in more detail. “I am cautiously optimistic, from the perspective of the audience, they should be too,” he said. “This is not a mouse study, it’s a people study. And that matters.”

 

Even if further trial results are positive, it is likely to be several years before the drug would become available on the NHS. Another phase-three trial is due to report in 2016 and then the drug would need to go through regulatory approval and would need to be shown to be sufficiently beneficial to patients.

 

About 225,000 people will develop dementia in the UK this year – a rate of one every three minutes.

 

Alzheimer’s Society research shows that 850,000 people in the UK have a form of dementia, and that in less than 10 years, 1 million people will be living with dementia. This is expected to rise to 2 million by 2051 unless preventative treatments are developed.

 

 

 

850,000 people in the UK have some form of dementia, including Alzheimer’s disease.

Photograph: Peter Byrne/PA

 

 

http://www.theguardian.com/science/2015/jul/22/scientists-find-first-drug-slow-alzheimers-disease

[Thaiexpat]

I have a better idea: DIET.

A diet rich in saturated fats has been shown to reverse the effects of this disease. Ketogenic diet ideas have been used successfully in this regard (and many other disease patterns). As Dr. Stein say so well in his website (neurosciencemyths.com) "A drug can never replace a nutrient. A nutrient can replace a drug"

Also remember (feel free to step in TD), the brain's energy organelles are easily damaged by oxidative stress/free radicals. anything you can do to limit/reduce/eliminate those will protect your brain from further damage.

Dunno, just saying....To your brain health

[tankdude]

I have a better idea: DIET.

A diet rich in saturated fats has been shown to reverse the effects of this disease. Ketogenic diet ideas have been used successfully in this regard (and many other disease patterns). As Dr. Stein say so well in his website (neurosciencemyths.com) "A drug can never replace a nutrient. A nutrient can replace a drug"

Also remember (feel free to step in TD), the brain's energy organelles are easily damaged by oxidative stress/free radicals. anything you can do to limit/reduce/eliminate those will protect your brain from further damage.

Dunno, just saying....To your brain health

 

Don't mind if I do - and yes, I feel this one is in my wheel house.

 

Let me start with this - http://www.ncbi.nlm.nih.gov/pubmed/20329590

 

"The human brain is nearly 60 percent fat. We've learned in recent years that fatty acids are among the most crucial molecules that determine your brain's integrity and ability to perform. Essential fatty acids (EFAs) are required for maintenance of optimal health but they can not synthesized by the body and must be obtained from dietary sources."

 

Hmmm....that certainly sounds like a good basis for a ketogenic diet to me. Speaking of a ketogenic diet, I found this great article on ketones and the brain -

 

http://blogs.scientificamerican.com/mind-guest-blog/the-fat-fueled-brain-unnatural-or-advantageous/

 

"Despite their superficial differences, many neurological diseases share one major problem – deficient energy production. During metabolic stress, ketones serve as an alternative energy source to maintain normal brain cell metabolism. In fact, BHB (a major ketone) may be an even more efficient fuel than glucose, providing more energy per unit oxygen used. A ketogenic diet also increases the number of mitochondria, so called “energy factories” in brain cells. A recent study found enhanced expression of genes encoding for mitochondrial enzymes and energy metabolism in the hippocampus, a part of the brain important for learning and memory. Hippocampal cells often degenerate in age-related brain diseases, leading to cognitive dysfunction and memory loss. With increased energy reserve, neurons may be able to ward off disease stressors that would usually exhaust and kill the cell."

 

"Due to its high fat nature, keto increases poly-unsaturated fatty acids (PUFAs, such as DHA and EPA, both sold over-the-counter as “brain healthy” supplements), which in turn reduces oxidant production and inflammation. Inflammatory stress is another “root of all evil”, which PUFAs target by inhibiting the expression of genes encoding for pro-inflammatory factors."

 

pro-inflammatory factors - which leads me to oxidative stress. Oxidative stress, in a nutshell, is essentially an imbalance between the production of free radicals and the ability of the body to counteract or detoxify their harmful effects through neutralization by antioxidants. Oxidative stress creates the Redox signaling ROS that creates the body's response of inflammation. (Yes - redox signaling is a real thing)

 

http://www.redoxsignaling.com/

 

So - we need to try an reach homeostasis - oxidative balance if you will.  In relation to Alzheimer's Disease and Oxidative stress - I present these.

 

http://www.sciencedirect.com/science/article/pii/S0925443900000405

 

"Oxidative balance is emerging as an important issue in understanding the pathogenesis of Alzheimer’s disease. Examination of Alzheimer’s disease brain has demonstrated a great deal of oxidative damage, associated with both hallmark pathologies (senile plaques and neurofibrillary tangles) as well as in normal appearing pyramidal neurons."

 

http://ajcn.nutrition.org/content/71/2/621s.full

 

"Research in the field of molecular biology has helped to provide a better understanding of both the cascade of biochemical events that occurs with Alzheimer disease (AD) and the heterogeneous nature of the disease. One hypothesis that accounts for both the heterogeneous nature of AD and the fact that aging is the most obvious risk factor is that free radicals are involved. The probability of this involvement is supported by the fact that neurons are extremely sensitive to attacks by destructive free radicals. Furthermore, lesions are present in the brains of AD patients that are typically associated with attacks by free radicals..."

 

So let me take this one more step - if the free radicals from oxidative stress are wrecking havoc - what can we do to help fight it. My theory - and many others - glutathione. I have shares some information on what glutathione is and what it does before - http://dinarvets.com/forums/index.php?/topic/169917-the-big-three-bodies-own-natural-antioxidants/?hl=glutathione

 

There is a direct link here - http://www.ncbi.nlm.nih.gov/pubmed/24496077

 

"AD is an unduly common form of dementia that exacts a heavy toll on affected individuals and their families. One of the emerging causative factors associated with AD pathology is oxidative stress. This AD-related increase in oxidative stress has been attributed to decreased levels of the brain antioxidant, glutathione (GSH)."

 

and they are looking at it for therapy too -

 

http://www.sciencedirect.com/science/article/pii/S0925443911002262

 

"Oxidative stress is a known characteristic of MCI and AD. Up regulation of endogenous antioxidants is vital in combating oxidative stress and thus helping to slow the advancement of MCI and Alzheimer disease. Glutathione is the most abundant and versatile endogenous antioxidant with many enzyme systems to enhance its function. NAC (FDA approved) and GCEE are known to increase glutathione in the brain and periphery and protect against ROS-producing substances in vivo. More research needs to be invested in GCEE, since it has no known harmful effects and by-passes the feedback inhibition cycle of glutathione. Increasing glutathione remains a promising therapeutic strategy to slow or prevent MCI and Alzheimer disease."

 

Here is a link on some ideas on how to raise glutathione levels - http://www.immunehealthscience.com/how-to-raise-glutathione.html

 

I - of course - have to say that I personally use a supplement that has been shown to raise Glutathione and catalase by at least 500%  in vitro - among other things...