It is noteworthy that THC is a considerably more effective inhibitor of AChE-induced [Abeta] deposition than the approved drugs for Alzheimer’s disease treatment, donepezil and tacrine, which reduced [Abeta] aggregation by only 22% and 7%, respectively, at twice the concentration used in our studies.
Waitwaitwhat? A drug was approved for the purpose of reducing AChE-induced Amyloid beta deposition, with an effect size of only 7%? That’s not effective at all! How did that happen?
Donepezil was never approved as an aid to prevention of Alzheimer’s or even as a treatment focused on the pathophysiology. The only thing it appears to be effective in (which is also its only FDA-approved use) is as symptomatic relief, in improving memory and cognitive symptoms in various stages of Alzheimer’s. It’s believed to do this by enhancing cholinergic neurotransmission in the brain (damage to these synapses is thought to be the reason for part of the cognitive damage done by Alzheimer’s). I believe that the prescribing information explicitly says that there is no evidence that it delays the progression of the disease. EDIT: that is correct, see 12.1 in the prescribing info
I haven’t looked in detail at tacrine, but IIRC its pharmacological rationale is the same as that of donepezil. (Also, all the regulatory information above is US-centric.)
Waitwaitwhat? A drug was approved for the purpose of reducing AChE-induced Amyloid beta deposition, with an effect size of only 7%? That’s not effective at all! How did that happen?
Donepezil was never approved as an aid to prevention of Alzheimer’s or even as a treatment focused on the pathophysiology. The only thing it appears to be effective in (which is also its only FDA-approved use) is as symptomatic relief, in improving memory and cognitive symptoms in various stages of Alzheimer’s. It’s believed to do this by enhancing cholinergic neurotransmission in the brain (damage to these synapses is thought to be the reason for part of the cognitive damage done by Alzheimer’s). I believe that the prescribing information explicitly says that there is no evidence that it delays the progression of the disease. EDIT: that is correct, see 12.1 in the prescribing info
I haven’t looked in detail at tacrine, but IIRC its pharmacological rationale is the same as that of donepezil. (Also, all the regulatory information above is US-centric.)