If there is anything more certain than the failure of experimental Alzheimer’s drugs — nearly 300, at last count — it is the immediate reaction of many diehard supporters of the amyloid hypothesis: They insist that idea, which served as the basis for most of those compounds, is still sound.
Roche pulls the plug on its anti-amyloid antibody crenezumab in January, after it has no chance of showing any benefit? Not enough to kill the amyloid hypothesis. Merck bails on verubecstat, which shut down production of toxic amyloid, in 2017? Still not enough. Eli Lilly announces in 2016 that its anti-amyloid solanezumab failed to show benefit in people with mild Alzheimer’s? Nope, not dead yet.
The same chorus was heard after Thursday’s terse announcement by Biogen and its partner Eisai that they were halting two clinical trials of the anti-amyloid aducanumab because it had basically no chance of showing effectiveness.
Neurodegenerative diseases are caused by bacterial infections which we don’t have the ability to document.
I have almost fully recovered from years of encephalitis from Lyme and underlying Epstein Barr. I think at one point I was actually dying. I was very deep and could barely communicate. I could not find my way home from the corner store without the maps on my iPhone. I fear Alzheimer’s every day and feel so sad for those who suffer and their families. The comment about about infections causing Neuro degenerative diseases makes sense.
Tengo 83 años y una esposa de 80, Ëlla tiene antecedentes personales de herpes labial y genéticos de y geneticos de de pérdida de memoria desde los 70 años; siempre leo con atención las publicaciones y/o investigaciones relacionadas con los problemas de memoria, demencia, Alzheimer; talvéz un tratamiento mas temprano con amiloide a personas con antecedentes genéticos podría beneficiarlos. Gracias por recibir esta sugerencia.
Have you considered “The Alzheimers Solution” 2017 by Dean & Ayesha Sherzai,MD at Loma Linda University Medical center.They discovered that the seventh-day adventists who were vegetarian did not have Alzheimers while those who ate meat and dairy protein did have Alzheimers. The the microvascular (capillary) endothelium is damaged by an animal based diet and protected by a whole food plant based diet high in fruits, vegetables and greens which are the source of essential micro nutrients. See “The China Study” 2nd edition 20016 by T Colin Campbell, Phd Cornell University. When the capillaries are damaged they cannot transmit oxygen and nutrients to the brain cells and reabsorb the waste products of metabolism and thus the waste products accumulate in the brain. This is also present in the retina of the eye where the waste products accumulate as drusen causing dry macular degeneration and eventually wet macular degeneration.
What if amyloid is the result of the disease, not the cause? Like a scab on a cut or burn, picking at the scab doesn’t help.
See also — https://news.harvard.edu/gazette/story/2017/05/devastating-chain-of-events-found-in-alzheimers-path/
In 2015, Wang YA in China, showed that all of the clinically failed monoclonal antibodies released toxic amyloid aggregates that were immobilized as plaque. Thus, while I agree with Tenzi’ comparison with a forest fire, I will go beyond, i.e. using those antibodies was like trying to kill a fire using gasoline. Also, there are myriad amyloid aggregates, thus, it is unlikely that a single antibody would work, maybe an assortment would. Aducanumab, may be effective, but only partially. What about using a combination of promising antibodies? That is what the body does. Finally, once Alzheimer’s starts, the damaging cascade also starts, i.e. amyloid triggers the phosphorylation of tau and its pathological effects. The problem is that once this process starts, it is apparent too late to stop by intervention at the amyloid level only. All of these facts have been known for years, i.e. in 1998, William Klein at Northwestern University showed unequivocally that the real villains in Alzheimer’s were the soluble amyloid-beta aggregates, later confirmed by various groups. Perhaps, Alzheimer’s research would benefit if the lessons of the past are taking into consideration and scientific writers look more into the science than the rock star status of their experts.
While there is clearly a need to better understand what causes the disease, we also need to look very closely at how we design the trials for treatments. The measures we use are largely unproven for the tasks for which they are being implemented. Also, we often enroll based on a cut off score, but where a person started before getting to that cut off matters a great deal; a person who was previously very high performing and has fallen to the cut-off is very different than someone who’s score was always at or near the cut-off.
Is anyone investigating possible disruption of blood brain barrier in AD patients? Toxins from leaky gut and fibrinogen from trauma would not be found in synapses if it were intact.
There’s a fair amount of research on Alzheimer’s and the blood-brain barrier, Eliseo. Here’s a link to published research with those terms as major topics: https://www.ncbi.nlm.nih.gov/pubmed?term=(%22Alzheimer+Disease%22%5BMajr%5D)+AND+%22Blood-Brain+Barrier%22%5BMajr%5D
2 studies using focused ultrasound for a sfae openning of the BBB of AD patients
Is it true Cannabis ameliorates inflammation? Professor Gary Wink, Ohio State University, says, “a puff a day keeps Alzheimer’s away”. He also states old mice given cannabis regain youthful vigor. He believes Cannabis given before symptoms of Alzheimer’s appears is prophylactic to this scourge. Any response to this comment would be greatly appreciated. Thank you. Joann M Horn, retired nurse, age 74
You may want to read the numerous publications of Prof. Micha Schwartz from the Weizmann Institute. Also, the recent ublication by an MIT team might pave a way for an effective energy-based (sound) intervention. This has been also shown previously with focused ultrasound
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