In a new study from the University of California San Diego, researchers developed a new method to screen drugs for treating Alzheimer’s disease.
Their work sheds light on why Alzheimer’s drugs so far have been ineffective at curing or reversing the disease and identifies new targets for drug development.
Drug development for Alzheimer’s has long been driven by the hypothesis that amyloid plaques—formed by the buildup of amyloid-beta proteins in the brain—are what kill neurons and cause Alzheimer’s.
As a result, many research efforts have focused on designing drugs that clear out these plaques.
In the study, the team developed a drug screening method that looks at what disease mechanisms, or endotypes, change in patients’ neurons as a result of treatment.
This is a new test for measuring whether an Alzheimer’s drug works.
The key here is that we are using the new mechanisms that we discovered to see how current drugs fail.
When drugs interact with human neurons, what things do the drugs fix, and what happens when they are not fixed in the process?
What’s also special about this method is that it screens drugs on actual patient cells.
The method involves taking human-induced stem cells derived from patients with familial Alzheimer’s disease, which is a hereditary form of Alzheimer’s, and transforming them into neurons.
The researchers treat these neurons with drugs and use next-generation sequencing techniques to evaluate the treatment.
The researchers also perform this drug screen on neurons derived from healthy individuals as a control experiment.
In this study, the researchers screened two experimental Alzheimer’s drugs that were designed to reduce or prevent the growth of amyloid plaques.
The researchers found that the drugs only fix some problems, such as the formation of amyloid plaques.
The drugs also partly fix the de-differentiation problem, by triggering “non-neuron” cells to transform back into neurons.
The findings suggest that fixing amyloid plaque formation does not reverse the disease in any way.
Once neurons de-differentiate into non-neurons, they lose their synaptic connections, which leads to loss of memory and cognition and as a consequence, dementia.
The team is excited to use these novel screening strategies for the Alzheimer’s drugs that are being developed in their laboratory.
Next, the researchers will evaluate their drug screening method on brain organoids.
The team will also work on developing new Alzheimer’s drug candidates and screening them with their method.
If you care about Alzheimer’s, please read studies about the likely cause of Alzheimer’s disease and new non-drug treatment that could help prevent Alzheimer’s.
For more information about brain health, please see recent studies about diet that may help prevent Alzheimer’s, and results showing that some dementia cases could be prevented by changing these 12 things.
The study is published in Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association and was conducted by Shankar Subramaniam et al.
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