From a Science article:
[Newly] published results from a closely watched clinical trial are being hailed as a big win by some in the Alzheimer's treatment field. The trial data hint that an anti–β amyloid antibody drug called aducanumab warded off cognitive decline in people diagnosed with early Alzheimer's. But the trial, an early test of the antibody's safety, is still too small to prove conclusive, leading many others to caution against false hope.
[...] newly published results from a closely watched clinical trial are being hailed as a big win by some in the Alzheimer's treatment field. The trial data hint that an anti–β amyloid antibody drug called aducanumab warded off cognitive decline in people diagnosed with early Alzheimer's. But the trial, an early test of the antibody's safety, is still too small to prove conclusive, leading many others to caution against false hope.
[...] Overall, Alzheimer's researchers are urging caution about the new drug results—even those who are co-authors on the paper. The study was "grossly underpowered" to determine whether cognition was actually better in people who took aducanumab, or a statistical fluke
Phase III trials are currently in progress and should be completed by 2020.
http://www.nature.com/nature/journal/v537/n7618/full/nature19323.html
https://clinicaltrials.gov/ct2/show/NCT02477800
https://en.wikipedia.org/wiki/Aducanumab
(Score: 2) by Post-Nihilist on Friday September 02 2016, @07:58PM
The question is rhetorical as there is no obscene amount of money to be made with a drug patented by the US government... from my favorite1 patent : Cannabinoids as antioxidants and neuroprotectants [uspto.gov].
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No signs of toxicity or serious side effects have been observed following chronic administration of cannabidiol to healthy volunteers (Cunha et al., Pharmacology 21:175-185, 1980), even in large acute doses of 700 mg/day (Consroe et al., Pharmacol. Biochem. Behav. 40:701-708, 1991) but cannabidiol is inactive at the NMDA receptor. Hence in spite of its potential use in treating glaucoma and seizures, cannabidiol has not been considered a neuroprotective agent that could be used to prevent glutamate induced damage in the central nervous system.
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It has surprisingly been found that cannabidiol and other cannabinoids can function as neuroprotectants, even though they lack NMDA receptor antagonist activity. This discovery was made possible because of the inventor's recognition of a previously unanticipated antioxidant property of the cannabinoids in general (and cannabidiol in particular) that functions completely independently of antagonism at the NMDA, AMPA and kainate receptors. Hence the present invention includes methods of preventing or treating diseases caused by oxidative stress, such as neuronal hypoxia, by administering a prophylactic or therapeutically effective amount of a cannabinoid to a subject who has a disease caused by oxidative stress.
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Therefore, CBD serves as a selective inhibitor of at least two lipoxygenase enzymes, 5-LO and 15-LO, but had no effect on 12-LO. Importantly, this is the first demonstration (FIG. 8) that the 12-LO product 12-HETE can play a significant role in protecting neurons from NMDAr mediated toxicity. Although the mechanism of this protection is unknown at the present time, 12-HETE is known to be an important neuromodulator, due to its ability to influence potassium channel activity.
The link between the previous quote and alz is 5-LO inhibition. 5-Lipoxygenase as an endogenous modulator of amyloid beta formation in vivo [nih.gov].
1It is my favorite patent as is it an irrefutable proof of the hypocrisy behind the war on cannabis and it's classification as a schedule 1 substance
Be like us, be different, be a nihilist!!!