Mice with a certain laboratory variant of Alzheimer’s disease have been shown to get much better with the use of an existing pharmaceutical. This is only in mice, only with a certain model of the disease, and is only one study, so we must be very cautious, but the results are on the face rather dramatic.
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Very cautious optimism is the correct response to this study. While the results are dramatic it’s worth remembering that the GM mice used in this study only model the amyloid-beta pathology of AD, and not other aspects of the disease such as the Tau pathology that also appears to play an important role. Indeed, given that the relative contributions of Tau and Amyloid beta – and for thaat matter the roles of different forms of amyloid beta and related peptides – are still not fully understood it is difficult to predict what effect this drug, assuming that it clears human beta-amyloid as effectively, will have on the progression of AD. Perhaps successful treatment of AD will require a drug combination that targets both the tau and amyloid beta pathways.
A down side of this publication is that there is already a lot of chatter on the internet about using bexarotene off-label to treat AD, which may lead to it being taken at incorrect doses by patients who would otherwise be contra-indicated for bexarotene. This puts the medical and research community in a difficult position, with the understandable clamor for it to be made available (and the numbers of charlatans no doubt lining up to make a quick buck off desperate patients and their families) are small-scale clinical trials to evaluate the safety and identify an effective dose range justified, given that this drug already has FDA approval? The researchers behind this work seem to think so, as they are already planning a small clinical trial involving 12 patients. It will be interesting to see if they get approval for this, of if their IRB seeks independent verification of their results first.
I guess we’ll soon find out.
I would go even farther in expressing caution. I am not optimistic at all. I think this result is purely artifact; a consequence of the mouse models they are using which are not at all like the natural disease in humans. These were transgenic mice that specifically over express amyloid and amyloid precursors. The adverse effects of amyloid in these mice are due to too much amyloid, and so it is not a surprise that removing amyloid makes them do better.
In humans most Alzheimer’s is not due to genes causing over expression of amyloid. There have been vaccination studies in humans where amyloid was completely cleared and there was no resolution of dementia.