Bexarotene, a cancer drug with a "... good safety and side-effect profile", quickly reversed amyloid plaque and symptoms of Alzheimer's disease in mice.
Our next objective is to ascertain if it acts similarly in humans. We are at an early stage in translating this basic science discovery into a treatment.
This is the most promising research I've seen, since this drug is already approved for use in cancer.
Drug effects in mice rarely show similar effects in humans, unfortunately. It's way too early to tell if this will be of any use. A primate trial would be required to see if this is even a plausible remedy; and even then, it's unlikely to reverse any damage.
Can't they compare cancer patients who took Bexarotene who also had early Alzheimers with noncancer Alzheimer's patients of similar age etc, just to look for an effect?
*Groan* It'll take them decades to get around to primate studies and then finish them, then do first stage human trials, then second stage trials, etc. By that time I'll be dead, or the economy will be so ruined nobody can afford the medicine.
I have heard that cures in mice seldom translate into human cures, something to the effect that every cancer researcher can cure cancer in mice.
Can't happen fast enough for me. About 85% of the residents in the nursing home where I work suffer from some form of dementia and staffing levels have been cut time and time again. We are struggling to cope with the work-load now so any relief would be more than welcome.
I heard a bit about this on NPR's Talk of the Nation - Science Fridays. Before that particular segment ended, the interviewee very emphatically stated: "Don't Try This At Home!" He indicated the possibility of negative side effects and emphasized that the effects in mice would not necessarily duplicate in humans. Certainly they have a mechanism they can look into and possibly duplicate in human subjects, but that is a LONG DISTANCE from a cure!
Resistance training slows mental decline.
Over the course of six months, the study team followed 86 senior women with probable mild cognitive impairment. The randomized controlled trial is the first to compare the efficacy of both resistance and aerobic training to improve executive cognitive functions necessary for independent living -- such as attention, memory, problem solving, and decision making. The trial also assessed the effect of both types of exercise on associative memory performance and corresponding functional brain plasticity.
The results showed resistance training significantly improved executive cognitive functions, associative memory performance, and functional brain plasticity. In contrast to previous studies in healthy older adults, aerobic training did not demonstrate any significant effect on cognitive function and brain plasticity.
"What our results show is that resistance training can indeed improve both your cognitive performance and your brain function. What is key is that the training will improve two processes that are highly sensitive to the effects of aging and neurodegeneration -- executive function and associative memory -- functions which are often impaired in early stages of Alzheimer's disease." [emphasis mine]
There's good news and bad news on Alzheimer's.
The bad news is that a form of "beta-amyloid, called pyroglutamylated (or pyroglu) beta-amyloid" is not only "up to 100 times more toxic" than regular beta-amyloid, it rapidly converts regular beta-amyloid to the hyper toxic form, kind of the way prion infection converts normal proteins into disease-causing ones, and then triggers the release of tau.
Bloom said the process is similar to various prion diseases, such as mad cow disease or chronic wasting disease, where a toxic protein can "infect" normal proteins that spread through the brain and ultimately destroy it. "You might think of this pyroglu beta-amyloid as a seed that can further contaminate something that's already bad into something much worse -- it's the trigger," Bloom said.
And the trigger fires a "bullet," as Bloom puts it. The bullet is a protein called tau that is stimulated by beta-amyloid to form toxic "tangles" in the brain that play a major role in the onset and development of Alzheimer's. ... the researchers found that without the interaction of toxic beta-amyloids with tau, the Alzheimer's cascade cannot begin.
The good news is
Probiodrug AG, based in Halle, Germany has completed phase 1 clinical trials in Europe with a small molecule that inhibits an enzyme, glutaminyl cyclase, that catalyzes the formation of this hypertoxic version of beta-amyloid.